Paramedian Pontine Infarction Research Articles

Influencing factors of early dramatic recovery of neurological function after intravenous thrombolysis in patients with branch atheromatous disease.

Intravenous thrombolysis can significantly improve the neurological function of patients with acute ischemic stroke. However, the expected early dramatic recovery (EDR) of neurological function after thrombolysis is not achieved in some patients with branch atheromatous disease (BAD). Here we evaluated the factors associated with EDR after thrombolysis in BAD patients. We conducted a retrospective study on 580 consecutive BAD patients. All patients met the diagnostic criteria of BAD and received intravenous recombinant tissue-type plasminogen activator (rt-PA). EDR was defined when the improvement of National Institutes of Health Stroke Scale (NIHSS) score was >8 points within 2 or 24 hours after rt-PA, or the total NIHSS score was 0 or 1. The factors associated with EDR were analyzed with multivariate logistic regression analysis. Among 580 patients, the incidence of EDR was 35.2% (204 cases). Compared with patients without EDR, patients with EDR had lower incidence of diabetes (15.7% vs 29.3%, P < .001), lower NIHSS scores at 2 and 24 hours after rt-PA (P < .001), less cerebral hemorrhage (0% vs 5.3%, P = .001), and shorter onset to treatment time (OTT) (P < .001). Multivariate logistic regression analysis in propensity score-matched cohort showed that EDR was associated with OTT (adjusted OR = 0.994; 95% CI, 0.989-0.999) and NIHSS score after rt-PA (adjusted OR = 0.768; 95% CI, 0.663-0.890). Notably, diabetes (adjusted OR = 0.477, 95% CI, 0.234-0.972) was an independent factor related to EDR of neurological function in BAD patients. In the subgroup analysis, a lower incidence of diabetes (adjusted OR = 0.205, 95% CI: 0.059-0.714, P = .013) and a lower NIHSS score after thrombolysis in patients with paramedian pontine infarction (adjusted OR = 0.809, 95% CI: 0.656-0.997, P = .047) were significantly associated with EDR. Diabetes is not conducive to EDR of neurological function in patients with BAD, especially in patients with paramedian pontine infraction. Low NIHSS score and short OTT after thrombolysis may be closely related to EDR after intravenous thrombolysis.

Morphological predictors of neurological deterioration in patients with acute isolated pontine infarct.

To investigate morphological predictors of neurological deterioration (ND) in patients with acute isolated pontine infarct. Acute isolated pontine infarct patients within 7days after onset of stroke symptoms were included retrospectively and classified into ND and non-ND groups. Morphological phenotypes (paramedian pontine infarct [PPI], atypical PPI, small deep infarct, and other types), topographical location, and lesion size were evaluated on axial diffusion-weighted imaging. There were 210 eligible patients, of whom 62 patients had ND (29.5%). The proportion of PPI was significantly higher in ND than that in non-ND (62.9% vs 39.6%). ND occurred more frequently in PPI patients than non-PPI patients (39.8% vs 20.5%). PPI located more frequently in lower pontine (20.4% vs 8.0%) and less in upper pontine (17.3% vs 30.4%, P = 0.028), and had larger ventro-dorsal length (13.8 ± 3.8 vs 9.9 ± 3.1) and width (8.3 ± 2.3 vs 6.2 ± 1.8) than non-PPI patients. The morphological phenotype of PPI was an independent risk factor for ND (OR 4.81, 95%CI 1.54-15.07, P = 0.007) in patients with isolated pontine infarct. The ventro-dorsal length of pontine infarct lesion was associated with ND (OR 1.18, 95%CI 1.01, 1.37, P = 0.034) in PPI patients. The morphological phenotype of PPI was a potential predictor for ND in patients with acute isolated pontine infarct. The ventro-dorsal length of pontine infarct lesion was possibly associated with ND in PPI patients.

Abstract Number ‐ 118: Compressive Vertebrobasilar Dolichoectasia: A Rare Etiology of Acute Pontine Ischemic Stroke Undeterred by Anticoagulation

Introduction Dolichoectasia is a term used to describe dilated, elongated and tortuous arteries due to defects within the medial layer of their walls secondary to loss of elasticity. Multiple pathophysiological processes might lead to the development of dolichoectatic vessels, and activation of metalloproteinases and irregular turbulent blood flow seem to cause irreversible disruption of the internal elastic lamina. Consequences often include mass effects and ischemic and hemorrhagic stroke. Blood flow within dolichoectatic arteries is turbulent predisposing to thrombus formation with resultant ischemic strokes. Ideally, with optimal anticoagulation therapy, such strokes can be prevented. However, in rare instances, they can still occur despite anticoagulation, likely due to direct compression of pontine perforators from dolichoectasias or persistent turbulent flow. Methods Case report Results A 66‐year‐old woman with hypertension, diabetes mellitus, atrial fibrillation (taking warfarin at home), and left‐sided trigeminal neuralgia due to compressive left vertebrobasilar dolichoectasia with a focal fusiform aneurysm, presented with transient dysarthria and lightheadedness lasting for less than an hour. MRI brain did not show any acute pathology. CTA head showed worsening left vertebrobasilar dolichoectasia with transitional fusiform aneurysm (24 mm in diameter) with mass effect on the anterior part of the pons and lower midbrain. Next day, the patient developed dysarthria and right‐sided weakness, and a repeat MRI brain showed a left acute paramedian pontine infarct. Warfarin was discontinued, and the patient was started on a heparin drip and later transitioned to Apixaban. Eventually, a diagnostic cerebral angiogram and surpass stent placement within the aneurysm were attempted which went uneventful and the flow through the aneurysm regularized. The patient was eventually discharged home on Apixaban and Prasugrel with interval follow‐up. Conclusions Compression of perforating vessels supplying brainstem structures, branching off the pathologic vertebrobasilar dolichoectasia is a rare etiology of acute pontine ischemic stroke, not with standing the anticoagulation. It warrants immediate neurosurgical intervention to optimize blood flow and prevent a recurrence.

Sequential pontine and bilateral cerebral peduncle infarction with resultant early Wallerian degeneration of the ponto‐cerebellar fibers

AbstractBilateral cerebral peduncular infarction (BCPI) is an extremely rare neurological disorder reportedly associated with locked‐in syndrome. A 60‐year‐old man represented with reduction in conscious level three weeks following a paramedian pontine infarction due to basilar artery thrombosis. Repeated MRI revealed subacute pontine infarction with new infarct involving bilateral cerebral peduncle. MRA showed absent flow‐related signal along the basilar artery consistent with occlusion. Additionally, Wallerian degeneration characterized by symmetrical hyperintense signal on MRI involving the ponto‐cerebellar fibers and both the middle cerebellar peduncles (MCPs) were seen. BCPI is an exceedingly rare type of stroke with characteristic symmetrical signal change involving the cerebral peduncles called “Mickey Mouse Ear” sign. Early Wallerian degeneration of the bilateral MCPs ensuing pontine infarction is also uncommon and is often detected incidentally and exhibits regular and symmetrical signal changes on MRI. Here, a rare encounter of early Wallerian degeneration following sequential pontine and BCPI is described.

Characteristics of basilar artery atherosclerotic plaques in pontine infarctions: A high-resolution magnetic resonance imaging study.

This study used a 3.0T high-resolution magnetic resonance imaging approach to explore basilar artery plaque characteristics in patients suffering from acute isolated pontine infarction. 30 consecutive patients suffering from acute isolated pontine infarction were enrolled in this study and underwent examinations including high-resolution MRI assessment of the basilar artery within 7 days following infarction. The basilar artery plaque burden of 16 patients with paramedian pontine infarction was 0.26±0.085, while the reconstruction index and enhancement rate index values in these patients were 1.097±0.133 and 1.750±0.447, respectively. In the 14 patients suffering from deep pontine infarction, these three values were 0.21±0.055, 0.896±0.223, and 1.285±0.611, respectively.These values differed significantly when comparing patients suffering from paramedian pontine infarction to those suffering from deep pontine infarction. This study suggests that the characteristics of basilar artery plaques differ between the two subtypes of pontine infarctions, which may account for the differences in prognosis associated with these two infarct subtypes.

Blood Pressure Variability and Severity of Early Prognosis in Patients with Acute Pontine Infarction.

Background Increased blood pressure (BP) variability may worsen the prognosis of stroke. This study aimed at investigating the association between BP variability and early functional prognosis in patients with pontine infarction. Methods According to types of pontine infarction, all the 137 patients were divided into two groups: 70 patients with paramedian pontine infarction (PPI) and 67 patients with deep pontine infarction (DPI). Common risk factors, 24-hour continuous blood pressure monitoring data, and the coefficient of variation were collected after admission in the hospital. Functional outcomes were evaluated with modified Rankin scale (mRS) at 3 months after discharge (favorable outcome: mRS scores ≤ 2; poor outcome: mRS scores > 2). Results The level of Glu, HbA1c, LDL, and NIHSS scores in the PPI group was significantly higher than that in the DPI group, and the concentration of blood uric acid was lower in the PPI group. Diastolic pressure in the PPI group is significantly higher than that in the DPI group, and coefficient of variation (CV) of systolic pressure in PPI is higher when compared with DPI ((88.77 ± 1.71) mmHg vs. (80.74 ± 1.31) mmHg; (11.54 ± 0.35) vs. (10.24 ± 0.25)). In multivariate analyses, the CV of systolic pressure, diastolic pressure, NIHSS scores, and the paramedian pontine infarction was independently associated with 3-month clinical outcome (OR = 1.94, 95% CI = 1.252–2.994, P=0.003; OR = 1.08, 95% CI = 1.002–1.166, P=0.04; OR = 1.58, 95% CI = 1.164–2.159, P=0.003; OR = 9.87, 95% CI = 1.045–32.193, P=0.04). Conclusion In conclusion, increased 24-hour (BP) variability, NIHSS scores, and paramedian pontine were associated with early poor prognosis in patients with acute pontine infarction.

Differentiation of Pontine Infarction by Size.

PurposeWe hypothesized that the current criteria may be unsuitable for lacunar pontine infarctions (LPI) diagnosis and that size criteria may indicate different stroke mechanisms.MethodsA total of 102 patients with isolated pontine infarctions were divided into a parent artery disease (PAD) and non-PAD groups according to stenosis of basilar artery. Further, 86 patients from the non-PAD group were divided into paramedian pontine infarction (PPI) and LPI groups. Data were collected from the three groups. The “golden” criterion for LPI was established based on the location of the infarction. A receiver operating characteristic (ROC) curve were used to evaluate the optimal cutoff value to use as an LPI diagnostic indicator.ResultsThere was a high prevalence of patients with PAD in both asymptomatic carotid atherosclerosis (ACAS) and PPI groups. Patients with PPI had a higher prevalence in diabetes and ACAS than those with LPI. Based upon the ROC curve, the optimal lesion size cutoff value for use as an LPI diagnostic indicator was 11.8 mm.ConclusionsDiffusion weighted imaging (DWI) cutoff points for predicting LPI may differ from that of the middle cerebral artery territory. The diameter of LPI may also indicate different stroke mechanisms.

Bilateral wallerian degeneration of the middle cerebellar peduncles secondary to pontine infarction: A case series

ObjectiveWallerian degeneration (WD) of middle cerebellar peduncles (MCPs) secondary to pontine infarction is rarely reported in the literature. Our aim in this study is to characterize its clinical and neuroradiological features. MethodsA retrospective review of 7 patients from a single institution was conducted. Only patients with pontine infarction and subsequent degeneration of the MCPs were included in the analysis. The features of clinical presentation and neuroimaging finding were summarized by our experienced neurologists. ResultsSeven patients (5 male, 2 female), ranging in age from 50 to 77 years, satisfied the inclusion criteria. All patients had cardiovascular risk factors and hypertension was the most common one. Almost all of the patients had hemiparesis and dysarthria, and could achieved good clinical outcome. On the initial scan, hyperintense on T2- and diffusion-weighted images suggested the acute pontine infarction. On the follow-up scan, however, hyperintensities of bilateral MCPs on T2-weight and FLAIR images were apparently demonstrated in all patients. The specific lesions in the MCPs were attributed to bilateral WD of the pontocerebellar fibres secondary to pontine infarction. ConclusionWD should be taken into account when patients are initially diagnosed with paramedian pontine infarction and follow-up MRI manifest as symmetrical hyperintense in the MCPs.

Abstract WP215: Role of Conventional Mri Brain for Basilar Artery Plaque Detection in Solitary Pontine Infarct

Background: Solitary pontine infarct is divided into paramedian pontine infarct (PPI) and small deep pontine infarct (SDPI). The novel high-resolution MRI is the current useful imaging method to characterize vessel walls and detect atherosclerotic plaques of the intracranial arteries. However, high-resolution MRI is not included in routine imaging protocol for patient with acute stroke. We intend to determine the role of conventional MRI and MRA of the brain in solitary pontine infarct. Material and Method: Fifty patients with pontine infarct undergo imaging study of MRI of the brain on T1-weighted image, T2-weighted image and post-gadolinium T1-weighted image (if available) to assess the presence of atherosclerotic plaque, and MRA of the brain using 3-dimensional time-of-flight MRA (3D TOF MRA) to assess the basilar artery luminography. Basilar artery assesses by axial T2-weighted image was scored as “presence of plaque” or “absence of plaque” and 3D TOF MRA of basilar artery is scored as “normal”, “irregular” or “stenosis” ≥ 30%. Pontine infarction is divided into paramedian pontine infarction (PPI) and small deep pontine infarction (SDPI) groups. Results: Fifty patients with pontine infarction are included, thirty-five with PPI and fifteen with SDPI. Conventional axial T2WI MRI of the brain detected basilar artery atherosclerotic plaques in about 50% of patients with pontine infarction: 51.4% (18 of 35 cases) in PPI and 46.7% (7 of 15 cases) in SDPI. No plaque is found in all cases of normal-appearing basilar luminography on 3D TOF MRA and plaque was identified in all patients with basilar artery stenosis on 3D TOF MRA. Conclusion: Basilar artery atherosclerotic branch disease is frequently detected in both groups of solitary pontine infarct (PPI and SDPI). Conventional MRI and MRA of the brain are the useful imaging methods that may characterize intracranial vessel wall abnormalities and may be helpful in further study of intracranial arterial diseases and in comprehension of stroke mechanisms.

Post-Stenotic Recirculating Flow May Cause Hemodynamic Perforator Infarction

Background and PurposeThe primary mechanism underlying paramedian pontine infarction (PPI) is atheroma obliterating the perforators. Here, we encountered a patient with PPI in the post-stenotic area of basilar artery (BA) without a plaque, shown by high-resolution magnetic resonance imaging (HR-MRI). We performed an experiment using a 3D-printed BA model and a particle image velocimetry (PIV) to explore the hemodynamic property of the post-stenotic area and the mechanism of PPI.Methods3D-model of a BA stenosis was reconstructed with silicone compound using a 3D-printer based on the source image of HR-MRI. Working fluid seeded with fluorescence particles was used and the velocity of those particles was measured horizontally and vertically. Furthermore, microtubules were inserted into the posterior aspect of the model to measure the flow rates of perforators (pre-and post-stenotic areas). The flow rates were compared between the microtubules.ResultsA recirculating flow was observed from the post-stenotic area in both directions forming a spiral shape. The velocity of the flow in these regions of recirculation was about one-tenth that of the flow in other regions. The location of recirculating flow well corresponded with the area with low-signal intensity at the time-of-flight magnetic resonance angiography and the location of PPI. Finally, the flow rate through the microtubule inserted into the post-stenotic area was significantly decreased comparing to others (P<0.001).ConclusionsPerforator infarction may be caused by a hemodynamic mechanism altered by stenosis that induces a recirculation flow. 3D-printed modeling and PIV are helpful understanding the hemodynamics of intracranial stenosis.

Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets.

ObjectivePerineuronal nets (PN) form a specialized extracellular matrix around certain highly active neurons within the central nervous system and may help to stabilize synaptic contacts, promote local ion homeostasis, or play a protective role. Within the ocular motor system, excitatory burst neurons and omnipause neurons are highly active cells that generate rapid eye movements – saccades; both groups of neurons contain the calcium-binding protein parvalbumin and are ensheathed by PN. Experimental lesions of excitatory burst neurons and omnipause neurons cause slowing or complete loss of saccades. Selective palsy of saccades in humans is reported following cardiac surgery, but such cases have shown normal brainstem neuroimaging, with only one clinicopathological study that demonstrated paramedian pontine infarction. Our objective was to test the hypothesis that lesions of PN surrounding these brainstem saccade-related neurons may cause saccadic palsy.MethodsTogether with four controls we studied the brain of a patient who had developed a permanent selective saccadic palsy following cardiac surgery and died several years later. Sections of formalin-fixed paraffin-embedded brainstem blocks were applied to double-immunoperoxidase staining of parvalbumin and three different components of PN. Triple immunofluorescence labeling for all PN components served as internal controls. Combined immunostaining of parvalbumin and synaptophysin revealed the presence of synapses.ResultsExcitatory burst neurons and omnipause neurons were preserved and still received synaptic input, but their surrounding PN showed severe loss or fragmentation.InterpretationOur findings support current models and experimental studies of the brainstem saccade-generating neurons and indicate that damage to PN may permanently impair the function of these neurons that the PN ensheathe. How a postulated hypoxic mechanism could selectively damage the PN remains unclear. We propose that the well-studied saccadic eye movement system provides an accessible model to evaluate the role of PN in health and disease.

Basilar plaque on high-resolution MRI predicts progressive motor deficits after pontine infarction

BackgroundThe association between progressive motor deficits (PMD) in acute pontine infarction and basilar stenosis is unclear. High resolution MRI (HRMRI) is an emerging tool for basilar artery evaluation and might provide more accurate information. We aimed to analyze the association between basilar plaque assessed by HRMRI and PMD after acute pontine infarction. MethodsWe identified consecutive patients with unilateral pontine infarction within 24 h of stroke onset. All the patients underwent diffusion weighted MRI, MR angiography and HRMRI within 24 h of admission. PMD was defined as an increase in National Institutes of Health Stroke Scale score by ≥ 1 during hospitalization. Factors potentially associated with PMD were validated by multivariate analyses. ResultsOf a total of 87 patients, 63 (72%) had paramedian pontine infarction (PPI) and PMD was observed in 28 (32%) patients. Apparent basilar plaque assessed by HRMRI was more frequent in those with PMD than in those without PMD (52% versus 33%, p < 0.001). In contrast, the frequency of basilar stenosis (>30%) assessed by MR angiography was similar regardless of PMD. In the patients with PPI, PMD was associated with hypertension and apparent plaque on HRMRI. After adjusting covariates, PMD was independently associated with apparent plaque on HRMRI (OR, 9.1; 95% CI 1.4–58.9). ConclusionsOur results suggest that basilar plaque assessed by HRMRI is associated with PMD in patients with acute unilateral pontine infarction. Since basilar stenosis may be underestimated by MR angiography, HRMRI may provide additional information for predicting PMD and evaluating basilar artery stenosis.

Arterial remodeling of basilar atherosclerosis in isolated pontine infarction.

Isolated pontine infarctions are usually classified as paramedian pontine infarction (PPI) and lacunar pontine infarction (LPI). Although they have different shapes and locations, some recent studies proved that they might both be associated with basilar artery atherosclerosis in pathogenesis. This study aimed to explore the difference of basilar artery remodeling between two subtypes of pontine infarctions. Patients with PPI or LPI were scanned by High-resolution MRI (HR-MRI). The MR images of patients with basilar artery atherosclerosis were further analyzed to measure the vessel, lumen and wall areas at different segments of basilar arteries. Stenosis rate and remodeling index were calculated according to which arterial remodeling was divided into positive, intermediate and negative remodeling. Vascular risk factors and remodeling-related features were compared between PPI and LPI, and also between patients with and without positive remodeling. 34 patients with PPI and 21 patients with LPI had basilar artery atherosclerosis identified by HR-MRI. Positive remodeling was dominant in LPI group while in PPI group, three subtypes of remodeling were equal. Patients with positive remodeling had higher levels of low-density lipoprotein and homocysteine. Positive remodeling of basilar artery might reflect the low stability of basilar atherosclerotic plaques, which was more closely associated with LPI than PPI.

Abstract W MP17: Basilar Plaque on High Resolution Mri Predicts Early Neurologic Deterioration After Pontine Infarction

Background: The association between early neurologic deterioration (END) in pontine infarction and basilar stenosis remains unclear. Recently, it has been reported that evaluation of the basilar artery using high-resolution MRI (HRMRI) could provide more accurate information about intracranial artery stenosis than MR angiography (MRA). We aimed this study to identify the relationship between basilar plaque assessed by HRMRI and END after pontine infarction. Methods: Ninety consecutive patients with unilateral pontine infarction within 24 hours of stroke onset were included. All patients underwent diffusion weighted MRI, MRA and HRMRI within 24 hours after admission. Basilar stenosis was assessed with MRA and HRMRI. Basilar plaque on HRMRI was classified as 1) "no plaque" when the wall of the basilar artery was clear; 2) "minimal plaque" when the basilar wall was irregular without clear crescentic thickening; and 3) "apparent plaque" when a typical lesion with a crescentic thickening of the wall could be seen. END was defined as increased NIHSS score by ≥2 during admission. Factors potentially associated with END were validated by multivariate analyses. Results: Sixty-six patients (73%) had paramedian pontine infarction (PPI) and 24 patients (27%) had deep pontine infarction (DPI). END was observed in 29 (32%) patients and they all had PPI. Patients with END had more frequent apparent plaque in basilar artery than without it (79% versus 33%, p=0.001). However, basilar stenosis (&gt;30%) assessed by MRA did not show any differences regardless of the presence of END (24% versus 17%, p=0.380). In univariate analysis with the patients with PPI, END was associated with hypertension (p=0.029) and apparent plaque (p=0.002). After adjusting covariates, END was independently associated with hypertension (OR, 6.672; 95% CI, 1.376-32.367) and apparent plaque (OR, 7.260; 95% CI 1.285-41.030). Conclusion: Our result suggest that basilar stenosis assessed by HRMRI was associated with END in patients with acute pontine infarction. However, the result was not significant when assessed by MRA. We suggest that since basilar stenosis are underestimated with MRA, HRMRI may be more useful in evaluating basilar artery stenosis and predicting END in pontine infarction.

Basilar Artery Atherosclerosis and Hypertensive Small Vessel Disease in Isolated Pontine Infarctions: A Study Based on High-Resolution MRI

Background: Isolated pontine infarctions are classified as paramedian pontine infarction (PPI) and lacunar pontine infarction (LPI), usually attributed to basilar artery (BA) atherosclerosis and small vessel disease (SVD), respectively. Recently, researchers found BA atherosclerotic plaques in LPI and made the pathogenesis of LPI confusing. Methods: We evaluated the presence and location of BA plaques with high-resolution MRI and SVD burden with presence of hypertension, leukoaraiosis and silent brain infarction. Results: The prevalence of BA plaques and SVD was similar between PPI and LPI, with most plaques relevant to corresponding infarctions. Some PPI had no plaques; some LPI had no obvious SVD. Conclusion: SVD and BA plaques with or without lumen stenosis were both possible causes of PPI and LPI.

Bruns-Cushing nystagmus due to hypertensive unilateral paramedian pontine base infarction

Bruns-Cushing nystagmus is unusually rare and is known to be related with cerebellopontine angle tumor. A 32-year-old male patient came to our emergency department 3 times because of dizziness, right upper limb ataxia, hypertension, and Bruns-Cushing nystagmus. Magnetic resonance imaging demonstrated left paramedian pontine infarction. In conclusion, Bruns-Cushing nystagmus not only indicates a cerebellopontine angle tumor but may also be associated with pontine infarction.

Fluctuating gustatory disturbance and ophthalmodynia heralding the onset of a paramedian pontine infarction

Lasting taste disturbance has been previously reported as a consequence of brainstem infarction, but there are no previous reports of transient gustatory sensations preceding the onset of stroke. Ophthalmodynia, presenting as “salt-and-pepper” eye pain, has been reported rarely. We present a 58-year-old right-handed woman who had fluctuating ophthalmodynia and taste disturbance immediately preceding a left paramedian pontine infarction. We discuss the neuroanatomical basis of taste in reference to this presentation.

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.

“Sixteen and a half”: a novel pontine neuro-ophthalmological syndrome

Two neuro-ophthalmological syndromes due to paramedian pontine infarction have previously been described. The ‘‘one and a half’’ syndrome was first reported and named by Miller Fisher [1], and consists of horizontal gaze palsy combined with an ipsilateral inter-nuclear ophthalmoplegia (INO) resulting in loss of all horizontal eye movements except abduction of the contralateral eye. The causative lesion is usually within the ipsilateral pontine tegmentum and is due to involvement of the abducens nucleus plus the medial longitudinal fasciculus (MLF), or alternatively to involvement of the MLF plus the paramedian pontine reticular formation (PPRF). These structures lie in close proximity to the nucleus and intra-axial fasiculus of the facial nerve. Consequently, ipsilateral fascicular lower motor neurone facial nerve palsy may accompany the ‘‘one-and-a-half’’ syndrome. This situation was named the ‘‘eight and a half syndrome’’ by Eggenberger [2], who reported 3 cases of this syndrome that had occured secondary to ischaemic stroke. In continuation of this concept, we here describe the ‘‘sixteen and a half syndrome’’, which is the ‘‘one and a half’’ syndrome with an additional 7th and 8th cranial nerve (vestibulo-cochlear nerve) palsy. A 78-year-old right-handed man presented with sudden onset of incomplete right upper limb paresis, horizontal diplopia and ataxia. This was shortly followed by complete right lower limb paresis. There was associated nausea and vomiting. Examination revealed a left-sided lower motor neurone facial nerve palsy and dysarthria with loss of conjugate gaze to the left and loss of adduction of the left eye. Abduction of the right eye was accompanied by horizontal nystagmus. Convergence was spared. The patient also complained of new-onset left-sided hearing loss. The patient and his family were certain that his hearing before this event had been normal. Magnetic resonance imaging (MRI) with diffusion-weighted sequences revealed an area of restricted diffusion consistent with an acute infarct. The lesion extended beyond and lateral to the paramedian pontine territory supplied by the anteromedial group of pontine perforating arteries, and dorsally to the fourth ventricle and the region of the facial colliculus (Fig. 1a, b). Pure tone audiometry showed no detectable hearing in the left ear. Brainstem auditory evoked potential testing showed no reproducible wave I, wave III or wave V after left ear stimulation. Waves I, III and V from right ear stimulation were of low amplitude with normal absolute and interwave latencies. Eight months later, the Weber test lateralized to the right ear, and the Rinne test revealed absent air-conducted and bone-conducted sound perception in the left ear. Our patient had an ‘‘eight and a half’’ syndrome plus additional ipsilateral hearing loss. We name this clinical entity the ‘sixteen and a half syndrome’. Hearing loss has not previously been described in association with either ‘‘one and a half’’ or ‘‘eight and a half’’ syndrome. A clinical series of 20 cases of ‘‘one and a half’’ syndrome noted G. Cummins R. Dunne K. O’Rourke (&) T. Lynch Dublin Neurological Institute, Mater Misericordiae University Hospital, 57 Eccles St., Dublin 7, Ireland e-mail: killian.orourke@gmail.com

Patient with pontine warning syndrome and bilateral posterior internuclear ophthalmoplegia: case report

BackgroundCapsular warning syndrome was first described in 1993, featured with repetitive episodes of motor and/or sensory dysfunction without cortical signs. Recently, it has been demonstrated that clinically typical capsular warning syndrome can be associated with pontine infarct and the term “pontine warning syndrome� was coined.Case PresentationA 54-year-old woman with a history of hypertension was seen with profound left-sided hemiplegia. She had had 3 episodes of left-sided weakness before complete hemiplegia. Her speech was slurred. Left central facial palsy and hemiglossoplegia were presented. Her left plantar response was extensor and bilateral posterior internuclear ophthalmoplegia was seen on neurologic examination. Biochemical tests revealed hyperglycemia and dyslipidemia on the next day. MRI demonstrated an acute right paramedian pontine infarct. The patient was commenced on oral clopidogrel, atorvastatin and acarbose. After 23 days of hospitalization, she was discharged with severe left hemiplegia.Conclusions1) Pontine warning syndrome may be underestimated and understudied. 2) Posterior internuclear ophthalmoplegia is a rare clinical sign in cerebrovascular diseases, while it can help to locate a brainstem lesion rather than an internal capsular one. 3) Blood pressure lowing administration may be improper for patients with pontine warning syndrome.