In our study, markers predicting END in patients with acute isolated pontine infarction were evaluated, and infarct volume and subtype-BABD were found to be strongly associated with END in API patients but not related to infarct location. Our study suggested that infarct volume may be a sensitive predictor in patients with isolated pontine infarction, especially BABD patients.
It has been reported that penetrating arterial infarction, especially pontine infarction, tends to progress to END, in contrast to cerebral deep penetrating artery infarction [1, 17]. Our study showed that 28.7% of the patients with isolated pontine infarction experienced END after admission, consistent with previous research findings, which reported an incidence of 27%~29% of END in API [1, 18]. In 1989, Caplan initially put forward the concept of BAD and proposed BA branch disease (BABD), which was defined as lesions extending to the ventral pontine surface in the blood supply region of the paramedian pontine artery with neither evidence of large arterial stenosis (> 50%) or occlusion nor evidence of cardiogenic embolism [19, 20]. In our study, BABD was responsible for 80.9% of END cases, and SVD accounted for only 19.1% (P < 0.001), indicating that the BABD subtype was associated with END in API, which was consistent with Gokcal’s et al.  study. A large retrospective study showed that BABD was the most common cause of API , accounting for 56.2% (86 of 153) of the APIs included in our study, and Yamamoto et al showed a relative frequency of approximately 40% . Our study did not compare long-term outcomes between BABD and SVD. However, Erro et al.  indicated that BABD patients have a worse prognosis than patients with lacunar pontine infarctions.
Our data show that the deterioration of symptoms was related to the maximum infarct volume (P = 0.002). Recently, a retrospective study that included 407 patients with API by Haiyan Li et al also found that infarct size might be a predictor for neurological progression with isolated acute pontine infarction (aOR 4.580, P < 0.0001), which was different from our study in which the infarct size was represented by the maximal data of the ventrodorsal length multiplied by rostrocaudal thickness. Interestingly, another study  suggested that END was not related to the size of either; however, its sample size was relatively small (n = 38), the expansion of ischemic lesions was not found to be correlated with END, and the actual lesion size was not measured.
Huang et al.’s  and Oh et al.’s  studies have shown that lower pons lesions may have a higher probability of progressive motor deficits in patients with isolated acute pontine infarction than those in the upper and middle pons. In Gokcal et al.’s  study, END was just numerically higher in patients with lower pontine infarction, but there was no statistically significant difference. Our multiple logistic regression data showed that the deterioration of symptoms was not related to lower pons lesions (P = 0.17), which was consistent with Li et al.’s  (P = 0.132) and Nakase et al.’s  conclusions. In addition, our study quantitatively analyzed the relationship between the distance between the lesion and the midline of the pons and END, and the results exceeded our expectations and were negative, which was consistent with Oh et al. , who qualitatively divided the patients into paramedian pontine infarcts and extended pontine infarcts according to axial lesion location.
In analyzing the relationship between END and infarct location and size in API from an anatomical point of view, the corticospinal tracts are loosely distributed along the corticospinal fibers in the upper pons, situated in the dorsolateral part of the pontine base at the level of the upper pons, and then converge into the anteromedial surface of the upper medulla to form compact bundles [23, 24]. Therefore, Huang et al.  and Oh et al.  thought that as a result of the corticospinal tracts in the lower pontine region being denser, typically in the paramedian ventral area, the damage to the corticospinal tracts is more serious. However, corticobulbar tracts are more widespread in the upper pons than in the lower areas of the pons . Therefore, from an anatomical point of view, the index reflecting the damage degree of the corticospinal tracts to the greatest extent should be the volume of the lesion rather than the location of the infarct. Both our study and Haiyan Li’s study showed that infarct volume was independently associated with END in API.
This study has the following limitations. First, it was a single-center retrospective study with a modest sample size. Second, repeat MRI was not performed after deterioration to determine whether there was infarct volume expansion in END patients and to identify the cause of the neurological deterioration. Third, our study did not compare the long-term functional outcomes of the two groups of patients.