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.
In vitro ischemia models have utilized oxygen, or oxygen and glucose deprivation to simulate ischemic neuronal injury. Combined oxygen and glucose deprivation can induce neuronal damage which is in part mediated through NMDA receptors. Severe oxygen deprivation alone however can cause neuronal injury which is not NMDA mediated. We tested the hypothesis that NMDA, or non-NMDA receptor mediated mechanisms may predominate, to induce neuronal injury following severe oxygen deprivation depending on the presence of glucose. We found that NMDA receptor blockade using dizocilpine (MK-801), DL-2-amino-5- phosphonovaleric acid (APV), or CGS 19755, was highly effective in reducing CA1 injury in organotypic hippocampal cultures, caused by complete oxygen and glucose deprivation. Complete oxygen deprivation alone however, caused CA1 neuronal injury which was not diminished using NMDA receptor blockade alone with MK-801 or APV, or in combination with AMPA/kainate receptor blockade using 6-cyano-7- dinitroquinoxalone-2,3-dione (CNQX). Neuronal protective strategies which act primarily through non-glutamate dependent mechanisms, including hypothermia, low chloride and calcium, and the free radical scavenger, alpha-phenyl-tert-butyl nitrone (PBN), provided neuronal protection against complete oxygen, as well as combined oxygen/glucose deprivation. Raising the pH using Hepes buffer during complete oxygen deprivation did not result in neuronal protection by NMDA receptor blockade. Partial oxygen deprivation alone, partial oxygen deprivation combined with glucose deprivation, glucose deprivation alone, and also glutamate exposure, all produced neuronal damage that was reduced by NMDA receptor blockade. The presence of glucose during complete oxygen deprivation appears to prevent glutamate receptor blockade from reducing neuronal injury in organotypic hippocampal cultures.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.