Predictors of Dysphagia in Acute Pontine Infarction
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Background and Purpose—Little is known about the frequency and the clinical characteristics of neurogenic dysphagia in pontine strokes. In this study, we sought to identify predictors for dysphagia in a cohort of patients with isolated pontine infarctions.
Methods—We included all patients admitted to our department between 2008 and 2014 having an acute (<48 hours after symptom onset) ischemic stroke in the pons, as documented by means of diffusion-weighted magnetic resonance imaging. Precise infarct localization was stratified according to established vascular territories. The presence of dysphagia was the primary end point of the study and was assessed by a Speech-Language Pathologist according to defined criteria.
Results—The study recruited 59 patients, 14 with and 45 without dysphagia. Median (interquartile range) stroke severity (in terms of National Institutes of Health Stroke Scale values) was higher in the dysphagic group as compared with patients without dysphagia (8.5 [6–12] versus 2 [1–5]; P<0.001). Infarct localization in the upper part of the pons (78.6% versus 33.3%; P=0.004) and in the anterolateral vascular territory (78.6% versus 31.1%; P=0.002) occurred more often in the dysphagic group. In a multivariate model, age, infarct volume, and National Institutes of Health Stroke Scale value were independent predictors of dysphagia.
Conclusions—Dysphagia occurs frequently in patients with isolated pontine infarctions. Clinical and imaging predictors of dysphagia may help to provide optimal screening, to prevent complications and to improve long-term prognosis.
Dysphagia is a common symptom among patients with acute ischemic stroke. It is associated with poor long-term outcome and increased mortality.1 Thus, early identification of patients at risk for swallowing disorders is of importance. Studies aimed to identify neuroanatomical predictors for dysphagia in acute stroke.2,3 They mostly focused on supratentorial infarctions and lesions in the medulla oblongata.4,5 However, stroke lesions in the pons are also frequently associated with dysphagia.6 Nevertheless, little is known about dysphagia in this type of infarction. This study included well-defined patients with isolated pontine infarctions. The aim was to define clinical variables and magnetic resonance imaging lesion patterns that are associated with dysphagia.
All patients admitted between 2008 and 2014 were screened for the presence of the following inclusion criteria: (1) diagnosis of acute ischemic stroke (International Classification of Diseases, Tenth Revision, I63.0-I63.9), (2) symptom onset to hospital admission <48 hours, and (3) presence of an isolated pontine infarction on magnetic resonance imaging (see Imaging Assessment below). Patients who received a computed tomographic scan only (for whatever reason) were not included. Patients with concomitant infarctions in other vascular territories were excluded (but patients having small spotty lesions in the cerebellum or in the posterior cerebral artery territory were allowed). Further exclusion criteria were: (1) age <18 years, (2) preexisting infarctions in the pons, (3) concomitant intracerebral hemorrhage, (4) preexisting dysphagia, and (5) concomitant diseases likely to cause dysphagia including dementia. Patients intubated at hospital admission or at immediate need of intubation were not included. However, intubated patients who were rapidly extubated after admission and patients who were intubated in the further course of the hospital stay were included. The study protocol was approved by the ethics committee of the University Hospital.
The following clinical variables were obtained: age (years), sex, stroke severity in terms of National Institutes of Health Stroke Scale (NIHSS) values, stroke pathogenesis according to the TOAST (Trial of Org 10172 in Acute Stroke Treatment) criteria, and vascular risk factors.
According to our in-house standard of practice, all patients received a full clinical swallowing examination within 24 hours after admission by an experienced Speech-Language Pathologist. Patients were classified as dysphagic if 2 out of the following 6 items were present: dysarthria, dysphonia, abnormal gag reflex, abnormal cough, cough after swallow, and wet voice (any 2 as described by Daniels et al7). Dysphagic patients subsequently underwent fiberoptic evaluation of swallowing for verification and severity quantification. Orofacial muscular symmetry, strength, and sensation as well as cranial nerve function were also assessed.
MRI was performed based on a standard in-house protocol. Brain images were independently rated by 2 scientists (W.P. and M.W.) who were blinded to the clinical parameters. Transversal and coronal diffusion-weighted imaging sequences delineating the ischemic tissue were used for analyses on infarct localization and infarct volume. Locations of infarcts were categorized according to a previously established anatomic map of vascular territories in the pons (anteriomedial, anterolateral, lateral, and posterior arterial territory).8 In addition, rostrocaudal location was classified into upper, middle, and lower pons. Two raters independently determined the largest diameter in all 3 planes and calculated lesion volume according to the (axbxc)/2 method9 (interrater Pearson correlation r=0.804; P<0.001). This method was chosen given the spheroid morphology of typical pontine infarctions.10 It is feasible with respect to its applicability in the clinical routine. Mean lesion volume was then derived from the 2 measurements. If volumetry deviated >50% between the 2 raters (n=9), a joint reevaluation was performed.
Statistical analyses were performed using IBM SPSS statistics, version 22 (Armonk, NY). Parametric data were compared using the t test and 1-way ANOVA. Categorical data were compared using the Mann–Whitney U test. χ2 test was used for comparison of binary data. Binary multivariate logistic regression analysis with simultaneous inclusion was applied to identify independent predictors of dysphagia.
Fifty-nine patients with acute pontine infarctions were included in this study. Mean age was 68±11 years, and 46% were female. Regarding stroke pathogenesis, more than half of the patients (54%) had a lacunar infarct, 7% were classified as cardioembolic and 27% as atherothrombotic. Twelve percent of the patients were treated with thrombolytic therapy in the acute phase. Baseline data and clinical variables of the study population are displayed in the Table.
Fourteen patients (24%) were classified as having dysphagia. NIHSS value at hospital admission and infarct volume were significantly higher in the dysphagic group as compared with the nondysphagic group, but no difference was found for age, sex, and vascular risk factors. Dysphagic patients more often had dysphonia, dysarthria, and facial palsies than nondysphagic patients (Table).
Regarding localization, we found an association between upper pontine infarctions as well as anterolateral infarctions and dysphagia. For all other localizations, the proportion of dysphagic and nondysphagic patients did not differ (Table; Figures 1 and 2). Mean infarct volume was 1.25±1.02 mL in patients with upper pontine infarctions, 0.80±0.89 mL in patients with middle pontine infarctions, and 0.97±1.2 mL in patients with lower pontine infarctions (1-way ANOVA P=0.175). Mean infarct volume was 1.14±1.06 mL in patients with anterolateral pontine infarctions, 1.26±1.30 mL in patients with lateral infarctions, and 0.76±0.86 mL in patients with anteromedial infarctions (P=0.116).
A multivariate logistic regression analysis revealed age, infarct volume, and NIHSS value at admission to be independent predictors of dysphagia (Table I in the online-only Data Supplement).
Our study demonstrated that dysphagia is a frequent finding in acute pontine infarctions. Clinical severity (in terms of NIHSS values), age, and infarct volume were identified as predictors of dysphagia in this type of stroke. Furthermore, lesion topography is of importance, as upper pontine and anterolateral infarcts more frequently lead to dysphagia than infarcts in other locations.
In contrast to the medulla oblongata and to supratentorial regions, the pons is not considered to contain a swallowing center.2 Thus, in pontine strokes, it is likely that the affection of corticobulbar projections leads to impaired swallowing. Anatomic literature considers these tracks to be more bundled in the upper areas of the pons and to be more widespread in the lower areas of the pons.11 This may well explain why dysphagia is particularly present in upper and anterolateral pontine infarctions. Our findings are in line with previous literature demonstrating that swallowing is dependent on the integrity of many regions in the rostral pons.12
Our study has limitations: first, the small number of patients limits the reliability of the multivariate statistical analyses. We, therefore, refrained from calculating more extensive models. Second, some patients with pontine infarction but without MRI might have been missed. This comprises the risk of a selection bias. On the other side, the homogeneous cohort of magnetic resonance imaging–confirmed pontine infarction is a strength of our study.
In conclusion, our data show that dysphagia is a frequent symptom among patients with pontine infarction. Patients should be carefully examined for the presence of dysphagia, in particular if NIHSS values are high and upper and anterolateral pontine areas are involved. This may prevent complications resulting from aspiration and may improve long-term prognosis. Further research including larger patient cohorts with additional instrumental dysphagia assessment is highly warranted.
The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.116.015045/-/DC1.
- Received September 23, 2016.
- Revision received January 10, 2017.
- Accepted February 17, 2017.
- © 2017 American Heart Association, Inc.
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