title: The effect of nimodipine on the evolution of human cerebral infarction studied by PET.
abstract: Fourteen patients were studied by positron emission tomography (PET) within 48 h of onset of a hemispheric ischemic stroke and again 7 days later. After the first set of PET scans, the patients were randomized to receive either nimodipine (n = 7) or a carrier solution (n = 7) by intravenous infusion. The infusions were maintained until the end of the second PET studies. CBF, cerebral blood volume (CBV), oxygen extraction ratio (OER), CMRO2, and CMRglc were measured each time. These metabolic and perfusion measurements were performed by standard methods. A surface map of each metabolic and perfusion measurement in the cortical mantle was generated by interpolating between the available slices. The various surface maps representing the physiological characteristics determined in the same or subsequent studies were aligned so that all data sets could be analyzed identically using an array of square regions of interest (ROIs). The functional status of each ROI was recorded at the two intervals following the cerebrovascular accident to characterize the evolution of the infarct, penumbra, and normal brain regions. We presumed the ischemic penumbra to be cortical regions in the proximity of the infarct and perfused at CBF values between 12 and 18 ml/100 g/min on the first PET scan, while densely ischemic regions had CBF of less than 12 nl/100 g/min and normally perfused brain greater than 18 ml/100 g/min. In the densely ischemic zone, CBF increased more in the nimodipine-treated group than in the carrier group. As well, in this region nimodipine reversed the decline in CMRO2 noted in the carrier group, the difference in the changes being significant. In the penumbra zone, comparable trends were noted in OER and CMRO2 but the difference in the changes between the two groups did not reach statistical significance. Changes in CMRglc and CBV were comparable between the two groups in both cortical regions.
authors.affiliation: McConnell Brain Imaging Centre, Montreal Neurological Institute, Quebec, Canada.
authors.forename: A M
authors.initials: AM
authors.lastname: Hakim
authors.forename: A C
authors.initials: AC
authors.lastname: Evans
authors.forename: L
authors.initials: L
authors.lastname: Berger
authors.forename: H
authors.initials: H
authors.lastname: Kuwabara
authors.forename: K
authors.initials: K
authors.lastname: Worsley
authors.forename: G
authors.initials: G
authors.lastname: Marchal
authors.forename: C
authors.initials: C
authors.lastname: Biel
authors.forename: R
authors.initials: R
authors.lastname: Pokrupa
authors.forename: M
authors.initials: M
authors.lastname: Diksic
authors.forename: E
authors.initials: E
authors.lastname: Meyer
mesh_terms: D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity / Q000187:drug effects; D002545:Brain Ischemia / Q000503:physiopathology; D002544:Cerebral Infarction / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009553:Nimodipine / Q000008:administration & dosage / Q000494:pharmacology*; D010477:Perfusion; D014055:Tomography, Emission-Computed
chemical_list: D009553:Nimodipine