Do Changes in Oxygen Metabolism in the Unaffected Cerebral Hemisphere Underlie Early Neurological Recovery After Stroke?

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Abstract
Background and Purpose Whether an initial depression of function in the unaffected hemisphere (“transcallosal diaschisis”) plays a role in early neurological recovery after acute stroke remains controversial. Previous studies were confounded by lack of acute-stage assessment with follow-up and by the problem of defining a suitable control group, since preexisting stroke risk factors may influence prestroke cerebral metabolism. We evaluated with positron emission tomography (PET) the relationships between unaffected-hemisphere (ie, contralateral) oxygen consumption (cCMRO 2 ) and quantitative neurological assessments (and their respective evolution over time) after ischemic stroke. Methods Among 30 consecutive patients with first-ever middle cerebral artery ischemic stroke studied with the 15 O equilibrium method, we selected all survivors (n=19; mean age, 74.6 years) who were investigated both within the first 18 hours after stroke onset (PET 1 ; mean, 11±4 hours) and 15 to 30 days later (PET 2 ; mean, 24±10 days), with each patient serving as his/her own control. Neurological deficits were quantified using Orgogozo's middle cerebral artery scale (N score) at each PET session. Neurological changes were calculated as changes in the N score. A late CT scan coregistered with PET provided infarct topography and volume index. Results At PET 2 , we observed the overall expected neurological recovery. There was a nearly significant trend for a decrease in cCMRO 2 from PET 1 to PET 2 , especially for the neocortex ( P =.08, F test); in a subgroup of eight patients with large infarcts, this CMRO 2 decline was significant ( P <.05) in the mirror region to the infarct. There was no significant correlation (Spearman's tests) between acute-stage cCMRO 2 and same-day N scores or between changes in cCMRO 2 versus changes in N score from PET 1 to PET 2 (any region). There was a nearly significant trend for lower PET 2 cCMRO 2 in the subgroup of eight patients with large compared with small infarcts ( P =.06). Conclusions We found no evidence for an influence of cCMRO 2 on acute-stage neurological deficit or for a role of the unaffected hemisphere in early recovery after acute MCA ischemic stroke. The decline in unaffected-hemisphere metabolism from the acute to the subacute stage in the face of overall clinical recovery appears clinically irrelevant. The fact that the neocortical cCMRO 2 at PET 2 tended to be lower, and declined significantly from PET 1 to PET 2 in the mirror region in the subgroup of patients with large infarcts, suggests that this delayed effect represents transcallosal fiber degeneration.