These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Positron emission tomography for the determination of pathophysiology of cerebral ischemia].
    Author: Herholz K, Heiss WD.
    Journal: Arzneimittelforschung; 1991 Mar; 41(3A):298-303. PubMed ID: 1859499.
    Abstract:
    Positron emission tomography (PET) measurements of regional cerebral blood flow, blood volume, oxygen extraction, oxygen consumption and glucose consumption permit a detailed investigation of the pathophysiology of cerebral ischemia. The magnitude of the reduction of oxygen consumption appears generally as most important for tissue viability. In general, cerebral blood flow is severely reduced at the onset of an acute ischemic stroke. Subsequently, a very variable increase of cerebral blood flow may be found, often as "luxury perfusion" of irreversibly damaged tissue or relative hyperperfusion which is most frequently seen in the periphery of an ischemic infarct. Measurements of cerebral blood flow without measurement of oxygen metabolism are therefore of limited value. Glucose metabolism is less reduced than oxygen metabolism in most cases, indicating substantial anaerobic glycolysis. In few cases very high fluorodeoxyglucose uptake can be seen as an indicator of massive lactate production, which may cause additional toxic tissue damage. In cases of chronic or transient ischemias two stages of cerebral vascular decompensation can be distinguished by measurements of local blood volume, blood flow and oxygen consumption: the first stage is characterized by vasodilatation of peripheral vessels, resulting an increased ratio of cerebral blood volume to cerebral blood flow; the second stage is characterized by decreased blood flow and increased oxygen extraction. Ischemic brain lesions frequently cause alterations of blood flow and metabolism also in remote brain areas, apparently due to neuronal functional inactivation of incomplete ischemic damage. Global metabolic alterations correspond to the general clinical impairment of patients, whereas asymmetric focal deactivations correspond frequently to neuropsychological deficits. Studies of metabolic activation by functional stimulation appear promising as a tool to assess therapeutic strategies for rehabilitation.
    [Abstract] [Full Text] [Related] [New Search]