Objective: To determine how cortical compensation occurs in higher cognitive systems during the recovery phase of diffuse axonal injury (DAI). Design: 12 right-handed patients with a magnetic resonance imaging (MRI) lesion pattern compatible with pure DAI were identified. Pure DAI was defined as finding of traumatic microbleeds on T2*-weighted gradient-echo images in the absence of otherwise traumatic or non-traumatic MRI abnormalities. 12 matched healthy controls were also enrolled. Functional magnetic resonance imaging (fMRI) was used to assess brain activation during a working memory test (Paced Visual Serial Attention Test (PVSAT)). Results: No significant group differences were observed in reaction times for the PVSAT. Although patients with pure DAI committed a few errors during the PVSAT, controls respond correctly to each probe. Controls showed activations in the left frontal gyrus, left parietal gyrus and right inferior parietal gyrus. Patients with pure DAI showed activations in the left inferior frontal gyrus, right inferior frontal gyrus and right middle frontal gyrus. Between-group analysis of the PVSAT task showed significantly greater activation of the right inferior frontal gyrus (BA 45) and right middle frontal gyrus (BA 9) in patient with pure DAI versus controls. Conclusions: Patients with pure DAI require compensatory activation of the contralateral (right) prefrontal region to carry out activities similar to healthy controls. These findings provide further evidence for the adaptive capacity of neuronal systems and brain plasticity during the recovery stages of DAI.

The correlations between changes in blood pressure after admission and hematoma expansion were in vestigated in 118 patients with spontaneous intracerebral hematoma admitted within 24 hours of onset who underwent serial computed tomography. Multiple logistic regression was performed to assess cor relations between hematoma enlargement and clinical characteristics on admission. Hematoma en largement was predominantly correlated with time of onset (p 0.01567), and not well correlated with blood pressure at admission (p 0.07908). Serial changes in blood pressure were investigated in 57 patients admitted within 6 hours of ictus whose blood pressures were monitored every hour from admission. Wilcoxon signedrank analysis was used to determine the relationships between hematoma enlargement and blood pressure. Patients with hematoma enlargement was significantly correlated with increased blood pressure (p 0.0004). Increases in blood pressure after admission may be a factor in hematoma enlargement.

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