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19 results of 4 texts with exact phrase : 'ischemic penumbra'.

1. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1 , , ,

apoptotic cascade, ischemic cascade, ischemic penumbra, neuroprotection, oligemia
apoptotic cascade, ischemic cascade, ischemic penumbra, neuroprotection, oligemia
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The infarct core, the ischemic penumbra and regions of oligemia have been visualized.
Recent studies of diffussion-perfussion weighted imaging in patients with stroke and TIA provide a new insighit into the pathophysiology of the focal cerebral ischemia. The infarct core, the ischemic penumbra and regions of oligemia have been visualized. The ischemic penumbra has been defined as an ischemic zone with reduced blood flow and absent bioelectrical activity, in which the ion homeostasis is not irreversibly disturbed. Initially, the ischemic penumbra in stroke patients has been demonstrated
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The ischemic penumbra has been defined as an ischemic zone with reduced blood flow and absent bioelectrical activity, in which the ion homeostasis is not irreversibly disturbed.
Recent studies of diffussion-perfussion weighted imaging in patients with stroke and TIA provide a new insighit into the pathophysiology of the focal cerebral ischemia. The infarct core, the ischemic penumbra and regions of oligemia have been visualized. The ischemic penumbra has been defined as an ischemic zone with reduced blood flow and absent bioelectrical activity, in which the ion homeostasis is not irreversibly disturbed. Initially, the ischemic penumbra in stroke patients has been demonstrated
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Initially, the ischemic penumbra in stroke patients has been demonstrated
Recent studies of diffussion-perfussion weighted imaging in patients with stroke and TIA provide a new insighit into the pathophysiology of the focal cerebral ischemia. The infarct core, the ischemic penumbra and regions of oligemia have been visualized. The ischemic penumbra has been defined as an ischemic zone with reduced blood flow and absent bioelectrical activity, in which the ion homeostasis is not irreversibly disturbed. Initially, the ischemic penumbra in stroke patients has been demonstrated
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Now the diffussion-perfussion MRI is widely used to demonstrate the ischemic penumbra and to follow when it proceed to cerebral infarction.
by positron emission tomography and it has been shown that the penumbra could last several hours after a symptom onset. Now the diffussion-perfussion MRI is widely used to demonstrate the ischemic penumbra and to follow when it proceed to cerebral infarction. It has been also shown that the penumbra in stroke patients can be a long-lasting perfussion abnormality. Thus, the visualization of the penumbra allows the treatment decision to be made on the base of the cerebral ischemia pathophysiology, but not on the duration of the neurological deficit. Recently, it has been pointed out that from pathophysiological viewpoint TIA could be defined as an ischemic penumbra of varied duration, which may proceed to cerebral infarction or reduce to oligemia. The neuroprotection in cerebral ischemia is designed to block different stages of the ischemic cascade and to attenuate the pathological apoptosis. The neuroprotective drugs belong to different pharmacological groups and possess various modes of action.
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Recently, it has been pointed out that from pathophysiological viewpoint TIA could be defined as an ischemic penumbra of varied duration, which may proceed to cerebral infarction or reduce to oligemia.
by positron emission tomography and it has been shown that the penumbra could last several hours after a symptom onset. Now the diffussion-perfussion MRI is widely used to demonstrate the ischemic penumbra and to follow when it proceed to cerebral infarction. It has been also shown that the penumbra in stroke patients can be a long-lasting perfussion abnormality. Thus, the visualization of the penumbra allows the treatment decision to be made on the base of the cerebral ischemia pathophysiology, but not on the duration of the neurological deficit. Recently, it has been pointed out that from pathophysiological viewpoint TIA could be defined as an ischemic penumbra of varied duration, which may proceed to cerebral infarction or reduce to oligemia. The neuroprotection in cerebral ischemia is designed to block different stages of the ischemic cascade and to attenuate the pathological apoptosis. The neuroprotective drugs belong to different pharmacological groups and possess various modes of action. They include inhibitors of glutamate release, antagonists of NMDA receptor, GABAA agonists, Ca
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Astrup J, Siesjo BK, Symon L: Thresholds in cerebral ischemia–the ischemic penumbra.
Astrup J, Siesjo BK, Symon L: Thresholds in cerebral ischemia–the ischemic penumbra.
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Pathophysiology of ischemic penumbra – revision of a concept.
Back T. Pathophysiology of ischemic penumbra – revision of a concept.
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Baron JC: Mapping the ischemic penumbra with PET: implications for acute stroke treatment.
Baron JC: Mapping the ischemic penumbra with PET: implications for acute stroke treatment.
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The ischemic penumbra: identification, evolution and treatment concepts.
Fisher M. The ischemic penumbra: identification, evolution and treatment concepts.
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Ginsberg MD: Injury mechanisms in the ischemic penumbra
Ginsberg MD: Injury mechanisms in the ischemic penumbra
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Beyond mismatch: evolving paradigms in imaging the ischemic penumbra with multimodal magnetic resonance imaging.
Kidwell CS, Alger JR, Saver JL. Beyond mismatch: evolving paradigms in imaging the ischemic penumbra with multimodal magnetic resonance imaging.
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Mapping the ischemic penumbra with PET: Implications for acute stroke treatment.
Baron JC. Mapping the ischemic penumbra with PET: Implications for acute stroke treatment. In: 7th European Stroke Conference, Edinburgh, 1998.
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Spontaneous neurological recovery after stroke and the fate of ischemic penumbra.
Furlan M, Marshal G, Viader GF, Derlon JM, Baron JC. Spontaneous neurological recovery after stroke and the fate of ischemic penumbra.
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From pathophysiological viewpoint he defines the TIA as a ischemic penumbra with different duration, which could proceed to cerebral infarct or reduce to benign oligemia and pointed out that TIA is an ideal target for rapid reperfusion and neuroprotection.
67 of which are printed in international journals or books and are widely cited, more than 800 citations. His method for quantitative evaluation of cerebral blood flow by impedance technique, known as “method of Hadjiev” in the international literature, has been published in “Progress in Brain Research” He introduces the concept of asymptomatic ischemic cerebrovacular disorders, published in books and papers, including in foreign journals. From pathophysiological viewpoint he defines the TIA as a ischemic penumbra with different duration, which could proceed to cerebral infarct or reduce to benign oligemia and pointed out that TIA is an ideal target for rapid reperfusion and neuroprotection. Author of guidelines for primary and secondary prevention of ischemic stroke. He is an Editor of textbooks and manuals of Neurology. Prof. D. Hadjiev has delivered lectures on cerebrovascular diseases and headache in Austria, Croatia and Turkey. He has conducted and supervised 10 dissertations and 9 of his post-graduate students are habilitated.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2012, No. 2 , , ,

The modern approach of treatment of ischemic stroke in the first hours of occurrence of the event refers to an early recanalization of thrombotic artery occlusion; avoiding the formation of infarction zone or limitation the process by recovering the brain perfusion in the area of the ischemic penumbra [1, 4, 6, 15].
The modern approach of treatment of ischemic stroke in the first hours of occurrence of the event refers to an early recanalization of thrombotic artery occlusion; avoiding the formation of infarction zone or limitation the process by recovering the brain perfusion in the area of the ischemic penumbra [1, 4, 6, 15]. Nowadays this target is achieved by intravenous or intra-arterial trombolysis with recombinant tissue plasminogen activator (rt-PA) within 3-4.5 hours of the stroke occurrence [1]. Hypothermia is not conventionally used method although it is known to reduce the infarct size by >40% when body temperature decreases to 34°C or below.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 1 , , ,

Hyperglycemia and stroke outcome: vindication of the ischemic penumbra.
Ginsberg MD. Hyperglycemia and stroke outcome: vindication of the ischemic penumbra.
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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 2 , , ,

Modern treatment in the first hours of the ischemic stroke onset is directed at early recanalization of arterial thrombus, prevention of an infarct zone formation or its limitation via reestablishment of brain perfusion within the area of the so-called ischemic penumbra (a borderline zone of decreased blood flow between the viable and the necrotic tissue).
Cerebrovascular diseases are a global medical and social problem because of their high morbidity, mortality and disability rate. Modern treatment in the first hours of the ischemic stroke onset is directed at early recanalization of arterial thrombus, prevention of an infarct zone formation or its limitation via reestablishment of brain perfusion within the area of the so-called ischemic penumbra (a borderline zone of decreased blood flow between the viable and the necrotic tissue). Nowadays, recanalization is achieved via venous infusion of recombinant tissue plasminogen activators (rt–PAs) up to 4.5 hours after the stroke onset, as well as via endovascular treatment including intraarterial thrombolysis, thrombaspiration, etc. We present a prospective cohort study: comparative evaluation of the outcome of the acute stroke treatment in patients hospitalized at the Second Neurological Clinic of the St Marina University Hospital – Varna, between 2011 and 2016, treated with/without intravenous thrombolysis.
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It is highlighted that this treatment can prevent the expansion of the thrombus to the ischemic penumbra; decrease the infarct size and the severity of the neurological deficit.
Undifferentiated treatment in the acute phase of ischemic stroke includes anticoagulants and antiplatelet agents. It is highlighted that this treatment can prevent the expansion of the thrombus to the ischemic penumbra; decrease the infarct size and the severity of the neurological deficit.
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