PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7749515

Hematologic disorders and ischemic stroke.

B B Weksler
View original source ↗Export metadata ↓

Abstract

Hematologic disorders that induce a thrombotic tendency contribute to overall ischemic stroke risk and may directly cause cerebral ischemia in patients without other risk factors. These disorders include platelet dysfunction, prothrombotic coagulopathies, defective fibrinolysis, abnormal red blood cell-vessel wall interactions, and antiphospholipid antibody syndromes. Multiple mechanisms promoting ischemia may underlie specific hematologic abnormalities. Improved markers for activation of platelets, coagulation and fibrinolysis are now being used to correlate prothrombotic mechanisms with ischemic pathology and, thus, to make therapeutic approaches more precise. Nevertheless, finding the ideal balance between preventing cerebral ischemia and incurring hemorrhagic toxicity remains difficult.

Explore related subjects

Brain IschemiaCerebrovascular DisordersHematologic DiseasesHumansRisk FactorsThrombolytic TherapyThrombosisJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B B Weksler. 1995. Hematologic disorders and ischemic stroke.. https://doi.org/10.1097/00019052-199502000-00007

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2004

Stroke following variceal sclerotherapy.

OBJECTIVE: Paradoxical embolism via a patent foramen ovale (PFO) has been identified as a potential risk factor for ischaemic stroke. Such occurrences are associated with risk factors for deep vein thrombosis (DVT), e. g. pregnancy, immobilisation, and surgery of the lower limbs. OBSERVATION: A 54-year-old otherwise healthy female presented with acute onset motoric aphasia and brachiofacial right hemiparesis. The cranial computed tomography showed a left striatal ischaemic infarction. The patient's history revealed a variceal sclerotherapy with polydocanol 0,5% three days prior to the onset of symptoms. Echovist TCM doppler revealed a right-to-left shunt. A patent foramen ovale (PFO) was detected by transesophageal echocardiography. There was no evidence of DVT in bilateral lower-extremity venous duplex ultrasound scanning. Other potential risk factors of stroke including thrombophilia could not be identified. The patient was treated with a high dose regimen of heparin and a further anticoagulation treatment was recommended. CONCLUSION: This case suggests a probable causal relationship between variceal sclerotherapy and paradoxical embolism resulting in a stroke. Variceal sclerotherapy might be a potential, but rare risk of embolism.

Brain Ischemia↗
PubMed2004

Cerebral neutrophil recruitment, histology, and outcome in acute ischemic stroke: an imaging-based study.

BACKGROUND AND PURPOSE: Evidence now exists for a pathogenic role for neutrophils in acute cerebral ischemia. We have studied the patterns and temporal profile of cerebral neutrophil recruitment to areas of acute ischemic stroke (IS) and have attempted to correlate this with neurological status and outcome. METHODS: Patients with cortical middle cerebral artery (MCA) IS were recruited within 24 hours of clinical onset. Neutrophil recruitment was studied using indium-111 (111In) troponolate-labeled neutrophils, planar imaging, and single-photon emission computed tomography (SPECT). Volume of brain infarction was calculated from concurrent computed tomography (CT). Hematoxylin and eosin sections were obtained postmortem (n=2). Outcome was measured using Barthel, Rankin, and National Institute of Health Stroke (NIHSS) scales. RESULTS: Fifteen patients were studied. Significant 111In-neutrophil recruitment to ipsilateral hemisphere, as measured by asymmetry index (AI), was demonstrated within 24 hours of onset in 9 patients; this response was heterogenous between patients and on repeated measurement attenuated over time. Histologically, recruitment was confirmed within intravascular, intramural, and intraparenchymal compartments. Interindividual heterogeneity in neutrophil response did not correlate with infarct volume or outcome. In an exploratory analysis, neutrophil accumulation appeared to correlate significantly with infarct expansion (Spearman rho=0.66; P=0.03, n=12). CONCLUSIONS: Neutrophils recruit to areas of ischemic brain within 24 hours of symptom onset. This recruitment attenuates over time and is confirmed histologically. While neutrophil accumulation may be associated with either the magnitude or the rate of infarct growth, these results require confirmation in future studies.

Brain Ischemia↗
PubMed2004

Recurrent stroke in patients with symptomatic carotid artery occlusion is associated with high-volume flow to the brain and increased collateral circulation.

BACKGROUND AND PURPOSE: To investigate whether the risk of recurrent ipsilateral ischemic stroke in patients with symptomatic carotid artery occlusion (CAO) is related to (1) volume flow in the contralateral internal carotid artery (ICA), basilar artery (BA), and middle cerebral arteries (MCAs), and (2) intracranial collateral flow to the symptomatic side, measured in the first 6 months after the qualifying symptoms occurred. METHODS: We prospectively studied 112 patients with symptomatic CAO. Quantitative volume flow was measured with magnetic resonance angiography (MRA) and collateral flow via the circle of Willis with MRA, via the ophthalmic artery (OA) with transcranial Doppler sonography, and via leptomeningeal anastomoses with conventional angiography. RESULTS: During 49+/-14 months of follow-up (mean+/-SD), 7 patients had recurrent ipsilateral ischemic stroke. Compared with patients without recurrent stroke, these patients had significantly higher total flow to the brain, ie, ICA+BA flow (mean 536 mL/min versus 410 mL/min; P<0.05), and significantly higher contralateral ICA flow (355 mL/min versus 209 mL/min; P<0.001), whereas BA and MCA flow showed no significant differences. Also, they more often had Willisian collateral flow (P<0.05), mainly caused by increased collateral flow via the posterior communicating artery (PCoA; 71% versus 28%; P<0.05), whereas collateral flow via the OA and leptomeningeal anastomoses did not differ significantly. CONCLUSIONS: Recurrent ipsilateral ischemic stroke in patients with symptomatic CAO is associated with high volume flow to the brain and increased collateral PCoA flow.

Brain Ischemia↗