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Paper title Crossed cerebellar diaschisis: diagnostic and prognostic value of MRI derived imaging - a BOLD-Cerebrovascular reactivity, MRI Perfusion and H2O-PET comparison study.
Paper code P36
  1. Christiaan Hendrik Bas van Niftrik Universitätsspital Zürich/ Universität Zürich Speaker
  2. Martina Sebök Universitätsspital Zürich/ Universität Zürich
  3. Oliver Bozinov Kantonsspital St. Gallen
  4. Marco Piccirelli Universitätsspital Zürich
  5. Susanne Wegener UniversitätsSpital & Universität Zürich
  6. Giuseppe Esposito Universitätsspital Zürich/ Universität Zürich
  7. Athina Pangalu Universitätsspital Zürich/ Universität Zürich
  8. Antonios Valavanis Universitätsspital Zürich/ Universität Zürich
  9. Alfred Buck Universitätsspital Zürich/ Universität Zürich
  10. Andreas Luft UniversitätsSpital Zürich
  11. Luca Regli UniversitätsSpital & Universität Zürich
  12. Jorn Fierstra Universitätsspital Zürich/ Universität Zürich
Form of presentation Poster
  • Joint SSNR | SSNS
Abstract text Introduction:
Crossed cerebellar diaschisis (CCD) refers to a reduction in cerebellar blood flow and metabolism contralateral to a supratentorial lesion, and corresponds to poorer clinical outcome. It is thought to be caused by an interruption of the cortico-ponto-cerebellar or the cerebello-thalamico-cortical fiber tracts. Positron Emission Tomography (PET) imaging is typically used to detect CCD, but advancing non-invasive MRI techniques such as dynamic susceptibility contract (DSC) MRI derived parameters or blood oxygenation-level dependent (BOLD) derived cerebrovascular reactivity (CVR) may prove be more optimal tools to characterize this disease. Hence, we aimed to study the novel diagnostic and prognostic potential of DSC-MRI and BOLD-CVR to detect CCD.

Nineteen subjects with symptomatic unilateral cerebrovascular steno-occlusive disease underwent a BOLD-CVR as well as a 15(O)-H2O PET study. Mean Transit Time, Time to Peak, relative cerebral blood flow and cerebral blood volume maps were derived from DSC-MRI. CCD as well as a cerebellar asymmetry index (CAI) were determined from PET. CAI was then also calculated for BOLD-CVR and all the DSC MRI derived maps separately and compared to PET CAI. Clinical status at admission and outcome after 3 months were determined with National Institute of Health Stroke Score (NIHSS) and modified Rankin Scale (mRS) scores.

CAI in CCD(+) subjects was significantly different for both BOLD-CVR and PET (CCD(+) vs. CCD(-) for BOLD-CVR: 14.76 ± 10.71 vs. 1.40 ± 5.43, p<0.001 and for PET: 7.04 ± 1.75 vs. 1.79 ± 3.14, p<0.001). No difference in CAI was seen for any of the DSC-MRI derived maps. The area under the curve (AUC) for BOLD-CVR was 0.88 (CI: 0.73-1.0). None of the DCS derived maps could accurately detect CCD with CBV showing the highest AUC of 0.6. Using a Cut-off value of 6.2 CAI for BOLD-CVR, CCD could be detected with a sensitivity of 0.87 and a specificity of 0.77. CCD(+) patients were in poorer clinical condition at baseline (CCD(+) vs. CCD(-): NIHSS: 6 vs. 1, p = 0.004; mRS: 3 vs. 1, p<0.01) and after 3 months follow-up (NIHSS: 2 vs. 0, p=0.03; mRS: 1 vs. 0, p=0.04).

In comparison to PET imaging, BOLD-CVR can accurately detect CCD, whereas none of the DCS MRI parameters proved to be able to characterize CCD. Furthermore, CCD(+) subjects had a significantly poorer initial clinical status and outcome after three months with both mRS and NiHSS scores.