Clinical spectrum of pontine infarction

Abstract

Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.

Topographic Location of Acute Pontine Infarction Is Associated With the Development of Progressive Motor Deficits

“…BA branch disease is the most common cause of stroke in patients with isolated pontine infarctions, with a relative frequency of about 40% 18,19 ; furthermore, these patients have a worse prognosis than patients with lacunar pontine infarctions. 20 Significant basilar artery stenosis, defined as reduction of the caliber of the basilar artery by at least 50% or occlusion of the basilar artery, was observed in 17.7% of our patients.…”

Multiple Pontine Perforator Infarction in Basilar Atherosclerosis

“…However, the main etiology of an unilateral multiple pontine infarction was not clear because of the paucity of case reports. 2 The TOF-MRA in this case showed no definitive stenosis from inherent limitations in showing the intraluminal pathology, but HR-MRI revealed an intraluminal atherosclerotic plaque with strong contrast enhancement ( Figure 2B, top) in the right posterolateral aspect of the basilar artery and stenosis at the orifice of the branching arteries (Figure 2A-B). The strong contrast enhancement of the plaque was reported to be associated with vulnerable phenotype and inflammatory process.…”

“…Seven slices of contrastenhanced T1-weighted axial images were obtained with following parameters: repetition time/echo time 850/10 msec, field of view 12 cm × 12 cm, thickness 2 mm, slice gap 0.3 mm, matrix 320 × 224, and number of excitations 4. Prolonged cardiac rhythm monitoring was also performed for three days and there was no evidence of atrial fibrillation.Previous vascular and topographic studies of pontine infarctions revealed etiologies of vascular topography as follows: [1][2][3] (1) anterolateral pontine infarction was usually caused by branch atheromatous disease of the basilar artery and (2) the tegmental pontine infarction usually arose from small artery disease. However, the main etiology of an unilateral multiple pontine infarction was not clear because of the paucity of case reports.…”

“…Previous vascular and topographic studies of pontine infarctions revealed etiologies of vascular topography as follows: [1][2][3] (1) anterolateral pontine infarction was usually caused by branch atheromatous disease of the basilar artery and (2) the tegmental pontine infarction usually arose from small artery disease. However, the main etiology of an unilateral multiple pontine infarction was not clear because of the paucity of case reports.…”

Intracranial Plaque Imaging Using High-Resolution Magnetic Resonance Imaging: A Pictorial Review

“…1) The infarction mechanism of basilar perforating artery territory can be divided into branch atheromatous disease, cardiogenic embolism, and small vessel disease. Especially, basilar branch atheromatous disease is the most frequent cause of basilar perforating artery territory infarctions (Bassetti et al, 1996;Kumral et al, 2002). Basilar artery atheomatous plaque can block at the orifice of the branch, or can extend into the perforating branch, which results in parapontine or deep pontine infarctions (Fisher & Caplan, 1971;Fisher, 1977).…”