The longitudinal changes of BOLD response and cerebral hemodynamics from acute to subacute stroke. A fMRI and TCD study

Claudia Altamura,Andreas Hetzel,Fabrizio Vernieri,Matthias Reinhard,Cornelius Weiller,Dorothee Saur,Farsin Hamzei,Magnus-Sebastian Vry,Christoph P Kaller,Paolo Maria Rossini

doi:10.1186/1471-2202-10-151

Abstract

BackgroundBy mapping the dynamics of brain reorganization, functional magnetic resonance imaging MRI (fMRI) has allowed for significant progress in understanding cerebral plasticity phenomena after a stroke. However, cerebro-vascular diseases can affect blood oxygen level dependent (BOLD) signal. Cerebral autoregulation is a primary function of cerebral hemodynamics, which allows to maintain a relatively constant blood flow despite changes in arterial blood pressure and perfusion pressure. Cerebral autoregulation is reported to become less effective in the early phases post-stroke.This study investigated whether any impairment of cerebral hemodynamics that occurs during the acute and the subacute phases of ischemic stroke is related to changes in BOLD response.We enrolled six aphasic patients affected by acute stroke. All patients underwent a Transcranial Doppler to assess cerebral autoregulation (Mx index) and fMRI to evaluate the amplitude and the peak latency (time to peak-TTP) of BOLD response in the acute (i.e., within four days of stroke occurrence) and the subacute (i.e., between five and twelve days after stroke onset) stroke phases.ResultsAs patients advanced from the acute to subacute stroke phase, the affected hemisphere presented a BOLD TTP increase (p = 0.04) and a deterioration of cerebral autoregulation (Mx index increase, p = 0.046). A similar but not significant trend was observed also in the unaffected hemisphere. When the two hemispheres were grouped together, BOLD TTP delay was significantly related to worsening cerebral autoregulation (Mx index increase) (Spearman's rho = 0.734; p = 0.01).ConclusionsThe hemodynamic response function subtending BOLD signal may present a delay in peak latency that arises as patients advance from the acute to the subacute stroke phase. This delay is related to the deterioration of cerebral hemodynamics. These findings suggest that remodeling the fMRI hemodynamic response function in the different phases of stroke may optimize the detection of BOLD signal changes.

Highlights

By mapping the dynamics of brain reorganization, functional magnetic resonance imaging MRI has allowed for significant progress in understanding cerebral plasticity phenomena after a stroke
The hemodynamic response function subtending blood oxygen level dependent (BOLD) signal may present a delay in peak latency that arises as patients advance from the acute to the subacute stroke phase
These findings suggest that remodeling the functional magnetic resonance imaging MRI (fMRI) hemodynamic response function in the different phases of stroke may optimize the detection of BOLD signal changes

Summary

Introduction

By mapping the dynamics of brain reorganization, functional magnetic resonance imaging MRI (fMRI) has allowed for significant progress in understanding cerebral plasticity phenomena after a stroke. The impact of brain area over-recruitment on functional recovery was investigated by longitudinal studies that tracked the evolution of such plastic changes over time [4,5,6] These studies found that there was an over-activation of certain brain areas (including supplementary areas and contra-lesional homologue areas) in the sub-acute phase followed by the progressive focusing of cerebral activation associated with clinical recovery [4,5,6]. In aphasic patients, this phenomenon was reported to have a tri-phasic trend from the acute to the chronic stage; the initially reduced cerebral activation was followed by an over-activation of the language cortical network in the subacute phase, which was followed by a progressive focusing of cerebral activation [7]

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