Acute Pontine Infarction Research Articles

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.

Diameter of the Basilar Artery May Be Associated with Neurological Deterioration in Acute Pontine Infarction

Purpose: The present study investigated the factors related to neurological deterioration in pontine infarction. Methods: Consecutive patients with acute pontine infarction without basilar artery (BA) occlusion were enrolled. Patients were classified into two groups (D, group with neurological deterioration; ND, group without neurological deterioration). After magnetic resonance angiography was performed to identify the diameters of internal carotid artery (ICA) and BA, the BA diameter/ICA diameter (BA/ICA) ratio was calculated. When the ischemic lesion on diffusion-weighted magnetic resonance imaging extended to the ventral basal pial surface, it was diagnosed as branch atheromatous disease (BAD). Results: Neurological deterioration occurred in 16 (31%) of 51 patients. BAD was found in 13 (81%) of 16 patients of the D group and 14 (40%) of 35 in the ND group (p = 0.008). The BA/ICA ratio was 0.73 (0.59–0.84) in the D group and 0.64 (0.55–0.71) in the ND group (p = 0.049). Multivariate regression analysis demonstrated that BAD (OR 15.62, 95% CI 2.37–103.13, p = 0.004) and a BA/ICA ratio of ≧0.70 (OR 7.76, 95% CI 1.55–38.88, p = 0.013) were independent factors associated with neurological deterioration. Conclusion: The BA diameter may be associated with neurological deterioration in acute pontine infarction.

Favorable Outcome From A Locked-In State Despite Extensive Pontine Infarction By MRI

Outcome prediction of patients who are in a locked-in state is challenging. Extensive pontine infarction on diffusion weighted imaging MRI (DWI) has been proposed as a poor prognosticator. We report on three patients with a locked-in state with unexpected favorable recoveries despite DWI evidence of widespread pontine ischemia. Report of three cases. Three young patients (32-, 30-, and 16-years-old) presented with a locked-in state caused by pontine infarction. The first patient did not receive any acute stroke therapies, the second patient underwent endovascular therapy 20 h after symptom onset resulting in partial recanalization of the basilar artery, and the third patient progressed to a locked-in state despite having received intravenous tissue plasminogen activator. The DWI of all three patients demonstrated acute and widespread pontine infarction involving more than two-thirds of the pons. Two patients regained full independence in their activities of daily living. The third patient remained wheelchair bound, but lives with her family, eats independently, uses a typewriter and wrote a book. Patients who are in a locked-in state may have substantial functional recovery despite DWI evidence of extensive pontine infarction.

Experience of Hyperbaric Oxygen Treatment on a Patient with Acute Ischemic Locked-in Syndrome

The characteristics of locked-in syndrome (LIS) are quadriplegia and anarthria with preservation consciousness. It is difficult to manage these symptoms. There have been several reports revealing the significant effectiveness of hyperbaric oxygen (HBO2) therapy on acute stroke, however, some journals show less favorable results using this treatment. There has also been no definite reporting of which lesions of the stroke are suitable for HBO2 therapy. We present a 65-yearold woman, suffered from acute ventral pontine infarction with LIS. Two days after onset, she received HBO2 therapy. One month later, she showed obvious functional recovery. There has been no previous published report discussing HBO2 therapy for acute ischemic pontine infarction. This is the first report regarding the obvious improvements of LIS using HBO2 therapy. Consequently, these findings suggest that HBO2 therapy could be used in conjunction with physical and rehabilitative therapy in the treatment of acute LIS for maximal functional improvement.

Vertebral artery dominance contributes to basilar artery curvature and peri-vertebrobasilar junctional infarcts

Objectives:The diameters of the vertebral arteries (VAs) are very often unequal. Therefore, this study investigated if unequal VA flow contributes to the development of basilar artery (BA) curvature and if...

Bilateral Horizontal Gaze Palsy with Unilateral Peripheral Facial Paralysis Caused by Pontine Tegmentum Infarction

Clinical features of pontine infarction depend on the topography of vascular lesion and most remarkably sometimes the same topographic region can lead to different clinical syndromes (e.g., dorsal pontine tegmentum). In this report we describe an elderly patient with acute dorsal pontine infarction leading to a unique syndrome of bilateral horizontal gaze palsy and unilateral peripheral facial paralysis. We propose that this syndrome could be included as a part of a continuum that involves one-and-a-half syndrome, eight-and-a-half syndrome, and other variants of pontine tegmentum infarction.

Acute Pontine Infarct in a 16-Year-Old Man with Acute Posterior Multifocal Placoid Pigment Epitheliopathy. A Case Report

A 16-year-old boy recently diagnosed with acute posterior multifocal placoid pigment epitheliopathy (APMPPE) developed an acute infarct in the left pontine region. No relevant abnormalities were found in the brain and cervical angiography, echocardiography, cerebrospinal fluid, and blood samples. Funduscopically, lesions were multiple circumscribed, creamy yellow patches, flat lesions at the level of the retinal pigment epithelium, and the fluorescence angiography confirmed an APMPPE. All visual and neurological symptoms reverted completely after use of steroid. Our patient is the youngest patient with APMPPE and stroke described so far, being the common age presentation between 20 to 40 years.

Locked-in or Comatose? Clinical Dilemma in Acute Pontine Infarct

A 50-year-old man presented after acute onset of dysarthria and tetraparesis, rapidly progressing to unresponsiveness. Neurologic examination revealed spontaneous ocular bobbing, pinpoint pupils with normal light response (top), extensor posturing, and bilateral Babinski signs. Loud noises, such as the clapping of hands, elicited a nonreproducible startle response evidenced by spontaneous eye opening. However, there were no eye movements on command. Computed tomography of the brain and magnetic resonance imaging showed evidence of an acute basilar artery thrombosis, also known as a hyperdense basilar artery sign (red arrow) and acute pontine infarction (middle). Electroencephalography showed presence of an α coma (bottom). Electroencephalography was helpful in determining the patient’s level of consciousness. Patients with locked-in syndrome have similar findings on neuroimaging studies, but awareness and eye movements are preserved and become the only means for communication. Electroencephalographic findings of an α coma indicate that the patient had impaired awareness and therefore did not have lockedin syndrome. α Coma after brainstem infarction was first described by Westmoreland et al1 in 1975. Normally, when patients’ eyes are closed, electroencephalography shows α activity in the posterior parts of the brain. In pathologic conditions, α activity emerges over all areas of the brain and remains whether eyes are open or closed. In this patient, coma resulted from a pontine infarction, which destroyed the ascending reticular activating system. Immediate and accurate assessment of consciousness in patients with acute pontine infarct is a very important task for clinicians.

Pontine Warning Syndrome

Little is known about stroke mechanisms in patients with fluctuating symptoms and the role of branch atherosclerotic disease. To report a novel stroke presentation associated with a paramedian pontine infarct due to branch disease with a fluctuating course. Case report. Academic research. Patient A 63-year-old man with hypertension, diabetes mellitus, and dyslipidemia was seen with fluctuating right-sided weakness and dysarthria. He had had 2 episodes of complete bilateral horizontal conjugate gaze palsy with unimpaired consciousness lasting for 5 minutes each. His pupils were 4 mm and were equal and reactive to light. Vertical gaze and convergence were preserved. His neurologic status fluctuated between 3 and 15 on the National Institutes of Health Stroke Scale. Results of computed tomographic angiography, perfusion, and magnetic resonance imaging. Intravenous tissue plasminogen activator was administered within a 3-hour window. Fluctuations in motor weakness persisted for 12 hours after receiving thrombolytic therapy. Neuroimaging showed an acute left paramedian pontine infarct with a patent basilar artery. Branch disease is a common mechanism in pontine infarctions. We coined the term "pontine warning syndrome" to characterize recurrent stereotyped episodes of motor or sensory dysfunction, dysarthria, or ophthalmoplegia associated with a high risk of imminent basilar artery branch infarction and a permanent deficit resembling those of capsular warning syndrome.

Concurrent Presentation of Perimesencephalic Subarachnoid Hemorrhage and Ischemic Stroke

Perimesencephalic subarachnoid hemorrhage (SAH) is a relatively benign form of SAH. The etiology of this condition is unknown but venous leakage has been believed to be the most likely cause. This report describes a patient with perimesencephalic SAH who presented with a concurrent acute pontine infarct demonstrated on diffusion-weighted magnetic resonance imaging. These findings suggest that in some instances perimesencephalic SAH is caused by rupture of a perforating artery.

Hemidystonia precipitated by acute pontine infarct

Hemidystonia is frequently due to an underlying structural lesion in the basal ganglia and thalamus. It has been suggested that a preserved corticospinal tract may be required for hemidystonia to manifest. We provide the first report of a patient who presented with rapid-onset hemidystonia precipitated by an acute pontine infarct demonstrated on diffusion-weighted magnetic resonance imaging. Acute dysregulation of pallidal efferents to the pedunculopontine and/or pontine afferents to the thalamus may precipitate hemidystonia.

Paramedian pontine infarction. Neurological/topographical correlation.

There have been few reports of pontine syndromes secondary to paramedian pontine infarctions. To clarify the clinicotopographical correlation and prognosis of paramedian pontine infarct syndromes, we analyzed the clinical signs and their association with MRI findings. We studied 49 patients with acute paramedian pontine infarcts and classified them into three subtypes on the basis of lesion location on MRI. Patient clinical status was assessed by Rankin Disability Scale (RDS) scores on admission and at 60 days after onset of stroke. Twenty-seven patients had basal infarcts. Clinical findings included dysarthria (n = 27), hemiparesis with upper extremity predominance (n = 15), brachial monoparesis (n = 4), and pathological laughing (n = 3). Fifteen patients had basal-tegmental infarcts. Clinical findings presented with hemiparesis and horizontal gaze abnormalities, including abducens nerve palsy (n = 1), internuclear ophthalmoplegia (INO) (n = 5), horizontal gaze palsy (n = 1), one-and-a-half syndrome (n = 1), and superficial or proprioceptive sensory dysfunction (n = 8). Seven patients had tegmental infarcts. Clinical findings included INO (n = 1), horizontal gaze palsy (n = 2), one-and-a-half syndrome (n = 3), and sensory changes (n = 2). On both admission and 60 days later, the RDS scores of the patients with upper pontine lesions were significantly better than those with lower pontine lesions (P < .01). The RDS scores of the patients with basal-tegmental infarct in the upper pons were significantly better than those with infarct in the lower pons (P < .02). Paramedian pontine infarcts, which are usually due to thrombosis of perforating arteries, presented with a faciobrachial dominant hemiparesis with dysarthria, somatosensory disturbance, and horizontal gaze abnormalities. The favorable outcome may be related to the level of the pontine lesion, which influences the effect on the corticospinal tract.

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.

Pontine infarction extending to the basal surface.

Etiology and symptomatology in pontine infarction extending to the basal surface are supposed to be different from those in deep pontine infarction of the lacunar type. The aim of this study was to compare the infarct size and location, vascular lesions, risk factors, and neurological deficits in three different types of acute pontine infarction. We studied isolated pontine infarction extending to the basal surface on brain imaging (group 1, n = 30), deep pontine infarction without extension to the basal surface (group 2, n = 23), and pontine infarction with simultaneous extrapontine infarct in the posterior circulatory system (group 3, n = 20). Clinical features, angiographic findings, and risk factors such as emboligenic heart disease, hypertension, and hypercholesterolemia were compared among the groups. The infarct area was 2.5 times greater in group 1 than in group 2. On angiogram, atherosclerotic stenosis of the basilar trunk was observed in 50% of the patients studied in group 1, in 0% in group 2, and in 78% in group 3. Emboligenic heart diseases were observed in 23%, 0%, and 30% in groups 1, 2, and 3, respectively. However, hypertension (60% to 65%), diabetes mellitus (35% to 45%), and hypercholesterolemia (13% to 17%) were equally distributed among the three groups. Classic lacunar syndromes were seen in 14 patients (47%) in group 1, in 20 patients (87%) in group 2, but in none of the patients in group 3. Patients belonging to group 1 showed a higher incidence of hemiparesis involving the face (37%), sensorimotor stroke (20%), and hemiparesis with confusion (17%) than those in group 2 (22%, 0%, and 4%, respectively) or in group 3 (0%, 5%, and 0%, respectively). Pontine infarction in group 1 may have several different causes, such as cardioembolism, artery-to-artery embolism, or atherosclerosis of the basilar artery affecting pontine branches. Severe neurological symptoms often result that differ from those seen in the deep pontine lacunar infarction in group 2.

Basilar branch pontine infarction with prominent sensory signs.

We identified 10 patients with acute pontine infarction and specific sensory findings. Two patients had pure sensory symptoms, two had sensory complaints of the hand and mouth, and the other six had hemisensory loss referable to medial lemniscal or spinothalamic tract dysfunction but localized to one limb, to an arm and leg, or to the face, characteristic of stroke localized to the cerebral hemisphere. All patients had magnetic resonance imaging showing infarction of the medial or lateral pontine tegmentum and a patent basilar artery. No definite source for cardiogenic thromboembolism was found. Infarcts in the midline extending from the base of the pons posteriorly into the tegmentum suggested basilar branch occlusion, while infarcts involving only part of the tegmentum probably resulted from small penetrator branch occlusion. Vertigo, light-headedness, or cranial nerve dysfunction suggested a pontine location of neurological dysfunction in these patients, but the nature of the sensory findings did not always predict the lateral, medial, inferior, or superior extent of tegmental infarction.