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Martin Lauritzen

Researcher at University of Copenhagen

Publications -  239
Citations -  19637

Martin Lauritzen is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Cerebral blood flow & Cortical spreading depression. The author has an hindex of 62, co-authored 227 publications receiving 17530 citations. Previous affiliations of Martin Lauritzen include New York University & Panum Institute.

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Glial and neuronal control of brain blood flow.

TL;DR: It is now recognized that neurotransmitter-mediated signalling has a key role in regulating cerebral blood flow, that much of this control is mediated by astrocytes, that oxygen modulates blood flow regulation, and that blood flow may be controlled by capillaries as well as by arterioles.
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Capillary pericytes regulate cerebral blood flow in health and disease

TL;DR: It is demonstrated that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes, which are major regulators of cerebral blood flow and initiators of functional imaging signals.
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Pathophysiology of the migraine aura. The spreading depression theory.

Martin Lauritzen
- 01 Feb 1994 - 
TL;DR: The combined experimental and clinical studies point to fruitful areas in which to look for migraine treatments of the future and provide a framework within which important aspects of the migraine attack can be modelled.
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Focal hyperemia followed by spreading oligemia and impaired activation of rcbf in classic migraine

TL;DR: The results indicate that the vasospastic model of the migraine attack is too simplistic and the normal rCBF increase during cortical activity was impaired in 6 patients.
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Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury:

TL;DR: Treatment strategies are suggested which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders.