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(Stroke. 2006;37:1525.)
© 2006 American Heart Association, Inc.

Original Contributions

Modest MRI Signal Intensity Changes Precede Delayed Cortical Necrosis After Transient Focal Ischemia in the Rat

Santiago Rojas, MSc; Abraham Martín, MSc; Carles Justicia, PhD; Carles Falcón, PhD; Núria Bargalló, MD, PhD; Ángel Chamorro, MD, PhD Anna M. Planas, PhD

From the Department of Pharmacology and Toxicology (S.R., A.M., C.J., A.M.P.), Institut d’Investigacions Biomèdiques de Barcelona (IIBB)-Consejo Superior de Investigaciones Científicas (CSIC), Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS); IDIBAPS (C.F.); Servei de Diagnòstic per la Imatge (N.B.), Hospital Clínic; and Stroke Unit (A.C.), Institut de Malalties del Sistema Nerviós (IMSN), Hospital Clínic, IDIBAPS, Barcelona, Spain.

Correspondence to Anna M. Planas, PhD, Department of Pharmacology and Toxicology, IIBB-CSIC, IDIBAPS, Rosselló 161, E-08036, Barcelona, Spain. E-mail ampfat{at}iibb.csic.es

Background and Purpose— Diffusion-weighted imaging (DWI) hyperintensities and apparent diffusion coefficient (ADC) hypointensities are MRI features of acute stroke. DWI alterations during ischemia recover with early reperfusion, but they can reappear later. Pronounced signal abnormalities early after stroke are associated with infarction, but the significance of subtle changes is unclear. Here we evaluated the degree and time course of regional signal intensity changes during the first 24 hours of reperfusion after transient ischemia, and we related them to the progression of the histopathological damage.

Methods— Rats (n=54) were subjected to 1-hour intraluminal middle cerebral artery occlusion to assess the dynamics of MRI signal intensity changes during the initial 24 hours and their correspondent histopathological features: 2,3,5-triphenyltetrazolium chloride (TTC) staining, and hematoxylin and eosin, and immunoreactivity to 70-kDa heat shock protein and to astroglial and microglial markers.

Results— This model of ischemia caused early striatal infarction but delayed necrosis in the cortex. The striatum showed marked MRI changes from 4 hours of reperfusion. By 12 hours, the striatal ADC signal intensity ratio to the homologous contralateral region was 30% reduced, and the TTC staining evidenced infarction. Contrarily, the cortical ADC ratio was only 15% reduced, and TTC staining was normal at 12 hours. After this time, the cortex showed sudden and pronounced (>30%) ADC signal intensity changes coincidentally with the manifestation of infarction, accompanied with severe vacuolation and unambiguous signs of neuronal and astroglial death.

Conclusions— These findings suggest that minor changes in ADC signal intensity early after ischemia should not be underestimated because they may be harbingers of delayed infarction.

Key Words: magnetic resonance imaging, diffusion-weighted • middle cerebral artery occlusion • neuronal death