Original Article

Journal of Cerebral Blood Flow & Metabolism (2006) 26, 696–707. doi:10.1038/sj.jcbfm.9600223; published online 21 September 2005

AC electrocorticographic correlates of peri-infarct depolarizations during transient focal ischemia and reperfusion

This work was supported by US Department of Defense funding.

Jed A Hartings1, Frank C Tortella1 and Michael L Rolli1

1Division of Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA

Correspondence: Dr JA Hartings, Division of Psychiatry and Neuroscience, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20910, USA. E-mail: jed.hartings@na.amedd.army.mil

Received 23 May 2005; Revised 25 July 2005; Accepted 2 August 2005; Published online 21 September 2005.

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Abstract

Several studies have highlighted a delayed secondary pathology developing after reperfusion in animals subjected to prolonged cerebral ischemia, and recently we have shown that peri-infarct depolarizations (PIDs) occur not only during ischemia, but also in this delayed period of infarct maturation. Here we study the electrocorticographic (ECoG) manifestations of PIDs as signatures of developing secondary pathology. DC- and traditional AC-ECoG signals were recorded continuously from epidural, nonpolarizable electrodes during 2 h of middle cerebral artery occlusion (MCAo) and 22 h of reperfusion in freely behaving rats. During MCAo, seizures and PIDs recurred frequently and their incidence was significantly correlated. After reperfusion, seizures and PIDs ceased, and for the next several hours delta wave abnormalities dominated the ECoG with progressively increasing amplitude. After a variable period (5 to 15 h), the ECoG amplitude decremented with the onset of a prolonged repetitive series of PIDs. Initial PIDs in this delayed phase produced transient depressions of the high amplitude ECoG signal, but thereafter the ECoG was persistently attenuated, with no transient depressions during subsequent PIDs. The time of onset of postreperfusion PIDs, and hence measures of ECoG attenuation, correlated with 24 h infarct volumes. PIDs could always be detected in baseline shifts of the AC-ECoG signal with a low high-pass cutoff setting. These results suggest that delayed PIDs after reperfusion contribute to a complex secondary pathology involving delayed edema, intracranial hypertension, and hypoperfusion. The manifestation of PIDs in ECoG/electroencephalography recordings may enable continuous real-time monitoring of infarct progression.

Keywords:

direct current potential, electrocorticography, focal cerebral ischemia, middle cerebral artery occlusion, peri-infarct depolarization, spreading depression

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