Isolated infarcts of the pons

Abstract

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.

Basilar Artery Atherosclerotic Plaques in Paramedian and Lacunar Pontine Infarctions

“…10,11 However, with the development of neuroimaging such as CT and MRI, large artery atherosclerosis (eg, BA stenosis) or cardiac thrombus have been identified as rare causes of pontine SDPI. 12 In our study, we showed that basilar atherosclerotic plaque could be in fact much more frequent in SDPI than previously thought. Our results were different from Fisher's pathological observation.…”

Characteristics of paramedian pontine arteries disease and its association with hemoglobinA1c

“…A mRS score of 6 was used for patients who died during the study period. Patients with FmRS ≤2 were considered to have a good outcome; patients with FmRS > 2 were considered to have a bad outcome (Bassetti et al., 1996) in PPD. Six months after stroke is the period for most functional recovery and is considered to be appropriate for assessing the outcome (Duncan, Jorgensen, & Wade, 2000).…”

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

“…7,11 Unilateral pontine infarctions usually manifest with lacunar syndromes, including pure motor stroke, ataxic hemiparesis, or dysarthria-clumsy hand. [12][13][14] Progression of motor weakness is relatively common in acute pontine infarction cases and is frequently associated with increased functional disability. 1 Recently, basilar artery (BA) stenosis was reported to be related to the subacute increase in lesion volume seen in pontine infarctions but was not correlated with clinical outcomes.…”