Basilar Artery Branch Disease Research Articles

Risk factors for early neurological deterioration in acute isolated pontine infarction without any causative artery stenosis

BackgroundThis study aimed to investigate the risk predictors for early neurological deterioration (END) in isolated acute pontine infarction without any causative artery stenosis.MethodsIn this retrospective study, patients with isolated acute pontine infarction within 72 h of symptom onset were enrolled between October 2017 and December 2021. END was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) score ≥ 2 points within the first week postadmission. Patients were divided into the END and the non-END groups. Multiple logistic regression analysis was used to evaluate independent predictors of END in patients with isolated acute pontine infarction.ResultsA total of 153 patients were included in the final study (62 females; mean age, 67.27 ± 11.35 years), of whom 28.7% (47 of 153) experienced END. Multiple logistic regression analyses showed that infarct volume (adjusted odds ratio [aOR], 1.003; 95% CI, 1.001–1.005; P = 0.002) and basilar artery branch disease (aOR, 3.388; 95% CI, 1.102–10.417; P = 0.033) were associated with END. The combined ROC analysis of the infarct volume and basilar artery branch disease for predicting END showed that the sensitivity and specificity were 80.9% and 72.6%, respectively.ConclusionBasilar artery branch disease and infarct volume were associated with END in acute isolated pontine infarction and may be useful prognostic factors for neurological progression.

Morphological classification of acute isolated pontine infarction and it's clinical relevance

Objective: To investigate a diffusion weighted imaging (DWI)-based morphological classification for acute isolated pontine infarcts (AIPI) and to assess differences in clinical characteristics, risk factors and functional outcomes among the different morphologies. Methods: All participants from SMART cohort with DWI-proven AIPI were included and categorized into 3 groups: basilar artery branch disease (BABD) group, small artery disease (SAD) group and large-artery-occlusive disease (LAOD) group, according to lesion extent of the transverse axial plane and basilar artery atherosclerosis severity. The clinical characteristics, vascular risk factors and 6-month's functional outcome was analyzed among 3 groups. Results: Of the 1 129 patients enrolled, 175 had AIPI. BABD was the most frequent subtype of AIPI (46.3%), followed by SAD (36.0%) and LAOD (17.7%). Neurological impairment on admission was more severe in the LAOD and BABD group than SAD group (P<0.001). In terms of risk factors, the percentage of hypertension was significant different among three groups (P<0.05). The average National Institute of Health stroke scale was 3.49 for SAD group, 5.93 for LAOD group, 5.97 for BABD group, and the differences were significant (P<0.001). The Poor outcome (mRS>2) was found in only 13.7% of patients at 6-month post-stroke and there was no difference among 3 groups. Conclusions: According to the morphological classification, BABD is the most frequent subtype of AIPI. The differences of the clinical characteristics and risk factors among three groups indicate that differences observed in morphology might have distinct pathophysiologic mechanisms. AIPI can be reliably classified based on morphology using clinical magnetic resonance images.

Atherosclerosis Might Be Responsible for Branch Artery Disease: Evidence From White Matter Hyperintensity Burden in Acute Isolated Pontine Infarction.

Objective: To investigate an MRI-based etiological classification for acute isolated pontine infarcts and to assess differences in vascular risk factors, clinical characteristics and WMH burden among the etiological subtypes.Methods: All participants from SMART cohort with DWI-proven acute isolated pontine infarcts (AIPI) were included and categorized into 3 groups: large-artery-occlusive disease (LAOD), basilar artery branch disease (BAD), and small vessel disease (SVD), according to basilar artery atherosclerosis severity and lesion extent of the transverse axial plane. The vascular risk factors and 6-month functional outcome was analyzed among 3 groups.Results: Of the 1129 patients enrolled, 175 had AIPI. BAD was the most frequent subtype of AIPI (46.3%), followed by SVD (36.0%) and LAOD (17.7%). Neurological impairment on admission was more severe in the LAOD group, followed by BAD. The BAD group had greater frequencies of female sex, hypertension, diabetes mellitus compared to the SVD group (P < 0.05). NIHSS on admission were significantly higher in the BAD group as compared with the SVD group (P < 0.001), but no difference was found between BAD and LAOD group. Poor outcome (mRS≥3) was found in only 13.7% of patients at 6-month post-stroke and there was no difference among 3 groups. WMH severity was significant higher in the SVD group compared to the BAD group for the deep subcortical region; however, there was no difference for the periventricualr region. There was no significant difference in either DWMH or PVWMH severity between the BAD and LAOD groups.Conclusion: BAD is the most frequent etiology of AIPI followed by SVD and LAOD. WMH burden, vascular risk factors and clinical characteristics in BAD group were more similar to the LAOD group, rather than to the SVD group, suggesting the atherothrombotic nature of BAD.

Progressive deficit in isolated pontine infarction: the association with etiological subtype, lesion topography and outcome.

It is important to predict progressive deficit (PD) in isolated pontine infarction, a relatively common problem of clinical stroke practice. Traditionally, lacunar infarctions are known with their progressive course. However, few studies have analyzed the branch atheromatous disease subtype as a subtype of lacunar infarction, separately. There are also conflicting results regarding the relationship with the topography of lesion and PD. In this study, we classified etiological subtypes and lesion topography in isolated pontine infarction and aimed to investigate the association of etiological subtypes, lesion topography and clinical outcome with PD. We analyzed demographics, laboratory parameters, and risk factors of 120 patients having isolated pontine infarction and admitted within 24h retrospectively. PD was defined as an increase in the National Institutes of Health Stroke scale ≥2 units in 5days after onset. Patients were classified as following: large artery disease (LAA), basilar artery branch disease (BABD) and small vessel disease (SVD). Upper, middle and lower pontine infarcts were identified longitudinally. Functional outcome at 3months was determined according to modified Rankin scores. Of 120 patients, 41.7% of the patients were classified as BABD, 30.8% as SVD and 27.5% as LAA. 23 patients (19.2%) exhibited PD. PD was significantly more frequent in patient with BABD (p 0.006). PD was numerically higher in patients with lower pontine infarction. PD was associated with BABD and poor functional outcome. It is important to discriminate the BABD neuroradiologically from other stroke subtypes to predict PD which is associated with poor functional outcome in patients with isolated pontine infarctions.

Stroke Subtypes and Topographic Locations Associated with Neurological Deterioration in Acute Isolated Pontine Infarction

This study investigated predictors of neurological deterioration (ND) in acute isolated pontine infarction. Two hundred fifty-nine patients with acute isolated pontine infarctions identified using diffusion-weighted imaging were retrospectively analyzed. The patients were divided according to the presence/absence of ND, defined as increased (≥2 units) National Institutes of Health Stroke Scale scores 5 days after onset. Pontine infarctions comprised 3 stroke subtypes: vertebrobasilar large-artery disease, basilar artery branch disease (BABD), and small-artery disease (SAD), according to basilar artery atherosclerosis severity and lesion extent of the transverse axial plane. Topographic locations of longitudinal pontine infarctions in the axial plane were divided into upper, middle, lower, and whole. Of the 259 patients (male : female = 136:123, 68.84 ± 10.24), only 27.4% exhibited ND. The prevalence was significantly increased in females, whereas smoking was significantly decreased in patients with ND. BABD and lower pontine infarctions were significantly more frequent in patients with ND (70.4% and 43.7%, respectively) than in patients without ND (51.6% and 30.3%, respectively). SAD and upper pontine infarctions were significantly less frequent in patients with ND (16.9% and 7.0%, respectively) than in patients without ND (30.3% and 23.4%, respectively). BABD and lower pontine infarctions were positively related to ND. This is the first study to demonstrate that BABD and lower pons lesions are predictors of ND in acute isolated pontine infarction. These findings indicate the potential importance of early identification of stroke subtypes and topographic locations in the prevention of ND in patients with suspected pontine infarction.

Clinical and imaging characteristics of isolated pontine infarcts: a one-year follow-up study

Objective: Although clinically relevant, there is paucity of literature regarding the characteristic findings and outcome in isolated pontine infarction (IPI). In this study, we examined and analyzed the association between neurological findings, imaging features, and outcomes at different time periods in patients with acute IPI.Methods: A total of 101 patients (32 women and 69 men) with IPI were included in this study. The data were prospectively collected within 7 days of stroke onset. A combination of diffusion-weighted imaging (DWI) and magnetic resonance angiography (MRA) was utilized for lesion analysis. Isolated pontine infarcts were categorized into three subtypes: large artery disease (LAD), basilar artery branch disease (BABD), and small artery disease (SAD). Patients were followed for 1 year to assess functional outcome and neurological deficit.Results: The most common type of IPI was BABD (53·5%). The baseline neurologic impairment was significantly more severe in the LAD and BABD groups than the SAD group (P = 0·002). Intracranial or extracranial arteriostenosis was dominated by LAD and was found in 44 patients (43·6%). Although 25·7% of patients had a poor outcome at 3 months post-stroke onset, their quality of life improved at the 1-year follow-up period.Discussion: Our study also provided the evidence that unilateral pontine infarction from BABD is the most prevalent subtype of IPI; the incidence of basilar artery stenosis was low; long-term prognosis was favorable.

Basilar Branch Occlusion

During the past few years, the branch syndromes have been ascribed to pontine lesions, and the development of neuroimaging techniques has renewed the interest in exploring their clinical-radiological correlation. Brain imaging via MRI has helped in the diagnosis and accurate localization of lesions. From classic studies it is now accepted that the pathogenic mechanism of lacunar pontine infarction (LPI) is perforating small arterial disease or microangiopathy caused by lipohyalinosis, whereas paramedian pontine infarction (PPI) are caused by paramedian or circumferential basilar branch disease due to atheromatous branch occlusion. The importance of basilar artery disease not only in severe posterior circulation infarcts but also in minor brainstem strokes is known from previous reports. The mechanism of PPI is probably local occlusion of the mouths of paramedian perforators through the atheromatous basilar artery (basilar branch occlusion). Infrequent basilar artery diseases such as dissection, aneurysm and hypoplasia, dolichoectatic basilar artery, embolism, or vasospasms are known to block the orifices of penetrating branch arteries and cause an infarct in the territory of the obstructed branches. An association between basilar artery branch disease and isolated pontine infarction exists; moreover, the enlargement of pontine lesion seems to be associated with neurologic worsening and fluctuating symptoms, but we know little about stroke mechanisms in patients with fluctuating symptoms and about the role of branch atherosclerotic disease. The treatment remains controversial, even in acute cases. Implementation of new neuroimaging techniques, such as high-resolution MRI, could be helpful in identifying pathogenetic mechanisms of isolated pontine infarction, thus improving therapeutic strategy and secondary prevention.

Progressive stroke in pontine infarction

The pathogenesis of isolated pontine infarctions is still unclear, being attributed both to small or large vessel disease. The extension of infarcted tissue to the pons surface has been indicated as a possible marker of basilar branch atheromatous disease and some neuroimaging evidence confirms this finding. On the basis of Kim's et al., study, we performed a revision of the literature addressing this topic. Several authors confirm an association between basilar artery branch disease and isolated pontine infarction; moreover, the enlargement of pontine lesion seems to be associated with neurological worsening. We therefore performed a brief analysis of possible mechanisms of progression. Prospective studies could be useful to evaluate predictors of neurological worsening in pontine stroke. Improvement of neuroimaging techniques is needed for a deeper comprehension of the etiopathogenesis of isolated pontine infarction.

Aetiopathogenesis and long-term outcome of isolated pontine infarcts

Isolated pontine strokes cause characteristic neurological syndromes and have a good short-term prognosis. The aim of this study was to examine the long-term survival, cumulative recurrence rate and clinical handicap of patients with isolated pontine infarcts of different aetiology. One hundred consecutive patients with an isolated pontine infarction were identified by imaging studies and evaluated prospectively. After extensive study, cases were classified according to the aetiopathogenetic mechanisms: stroke due to basilar artery branch disease (BABD), small-artery disease (SAD) and large-artery-occlusive disease (LAOD). During a mean follow-up period of 46 months, stroke presentation and initial course, early and long-term mortality, disability and recurrence were evaluated. BABD was the most frequent cause of isolated pontine ischaemia (43%), followed by SAD (34%) and LAOD (21%). Hypertension was the most prominent risk factor, especially among patients with SAD (94.1%). Neurological impairment on admission was more severe in the LAOD group, followed by BABD. After 1 month patients with LAOD had the highest cumulative mortality (14.3%, p = 0.026) and more severe disability (61.1%, p = 0.001). Five-year mortality rate was 20.6%, 14% and 23.8% in the SAD-, BABD- and in LAOD-group respectively (p = 0.776). Cumulative 5-year recurrence rate was 2.3 % for BABD, 14.3 % for LAOD, and 29.4 % for SAD (p = 0.011). Overall long-term survival of patients with isolated pontine infarcts is good. Initial differences regarding short-term outcome in infarctions of different aetiology resolve with time. Effective secondary prevention among SAD patients may limit stroke recurrence and positively influence long-term prognosis.

Clinical spectrum of pontine infarction. Clinical-MRI correlations.

We sought clinical and radiological findings of 150 consecutive patients with acute isolated pontine infarct who were admitted to our Stroke Unit over 6 years. In all patients CT, MRI and magnetic resonance angiography (MRA) were performed during the hospitalization. On clinico-radiological analysis regarding the pontine lesion boundaries there were five main clinical patterns that depended on the constant territories of intrinsic pontine arteries: (1). anteromedial pontine syndrome (58%) presented with motor deficit with dysarthria, ataxia, and mild tegmental signs in one third of patients; (2). anterolateral pontine syndrome (17%) developed with motor and sensory deficits in half of the patients, and were associated with tegmental signs (56%) more frequently than the anteromedial infarct syndrome; (3). tegmental pontine syndrome (10%) presented with mild motor deficits and associated with sensory syndromes, eye movement disorders and vestibular system symptoms including vertigo, dizziness and ataxia; (4). bilateral pontine syndrome (11%) consisted with transient consciousness loss, tetraparesis and acute pseudobulbar palsy; (5). unilateral multiple pontine infarcts (4%) were rarely observed, and were always associated with severe sensory-motor deficits and tegmental signs. In our series, there was no infarct in the extreme dorsal and lateral tegmental pontine territories which have been mostly associated with cerebellar infarctions. The main etiology of stroke was basilar artery branch disease (BABD) in 59 patients (39%), followed by small-artery disease (SAD) in 31 (21%), large-artery disease of vertebrobasilar arteries in 27 patients (18%), cardioembolism in 12 (8%) and in 16 patients (11%) no cause of stroke was found. Our findings suggest that it is possible to identify clinical subgroups of pontine infarction, in which BABD and SAD were the most common causes of stroke. After an acute onset, outcome is in general excellent except in those with bilateral pontine lesions.

Isolated infarcts of the pons.

We studied 36 patients with MRI-proven isolated acute pontine infarct. Corresponding to the constant territories of intrinsic pontine vessels, infarcts followed a predictable distribution, enabling us to delineate three main syndromes. Twenty-one patients had a ventral pontine infarct. Motor involvement varied from mild hemiparesis (ventrolateral pontine syndrome) to severe hemiparesis with bilateral ataxia and dysarthria (ventromedial pontine syndrome). In addition, three-fourths of the patients had clinical evidence for usually mild tegmental dysfunction. Eleven patients had a tegmental pontine infarct, presenting tegmental signs (eye movement disorders, cranial nerve palsies, sensory disturbances), and mostly mild motor deficits (tegmental pontine syndrome). Only four patients had alternating deficits, and these never corresponded to any of the so-called classic pontine syndromes. Infarcts in the medial and the extreme lateral tegmental territory were never observed in isolation, being always associated with cerebellar or larger (and multiple) infarctions in the posterior circulation. Four patients with a bilateral ventrotegmental pontine infarct presented with acute pseudobulbar palsy, bilateral motor deficits, and tegmental signs. The results of etiologic work-up emphasize the concept of basilar artery branch disease, which was the most common presumed cause of stroke (16/36, 44%). Basilar artery branch disease was particularly associated with large ventral infarcts, severe clinical symptomatology, progressive or fluctuating course, and local recurrence. Presumed small-artery disease (9/36, 25%) was usually associated with small ventral or tegmental infarcts and rapidly improving lacunar syndromes. Large-artery stenosis (8/36, 22%) and cardioembolism (1/36, 3%) were less common than in series of posterior circulation infarcts that include simultaneous pontine and extrapontine lesions. Recovery was good in two-thirds of the patients, the worse outcome being associated with large ventral infarcts.