Too many big words to understand anything here.
Delayed cerebral atrophy after cerebellar stroke: topographical relation and clinical impact
Running title: Remote impact of cerebellar stroke
Christiaan H.B. van Niftrik1,2*, Thomas F. Visser1,2,3*, Martina Sebök1,2, Giovanni Muscas4
,
Mohamad El Amki2,5, Carlo Serra1,2, Luca Regli1,2, Susanne Wegener2,5, Jorn Fierstra1,2
*Contributed equally to this paper
Affiliations:
1 Department of Neurosurgery, University Hospital Zurich, University of Zurich, Switzerland
2 Clinical Neuroscience Center, University Hospital Zurich, University of Zurich,
Switzerland
3 Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, UMC Utrecht,
Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
4 Department of Neurosurgery, Careggi Hospital and University of Florence, Florence, Italy
5 Department of Neurology, University Hospital Zurich, University of Zurich, Switzerland
Corresponding author:
Christiaan Hendrik Bas van Niftrik, MD, PhD
Department of Neurosurgery, University Hospital Zurich
University of Zurich
Frauenklinikstrasse 10
CH-8091 Zurich, Switzerland
Phone: +41-44-2551111
Fax: +41-44-2554505
E-mail: bas.vanniftrik@usz.ch
Page 1 of 26 Manuscripts submitted to Brain Communications
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© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium,
provided the original work is properly cited.
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Abstract
Remote dysconnectivity following cerebellar ischemic stroke may have a negative impact on
supratentorial brain tissue. Since the cerebellum is connected to the individual cerebral lobes
via contralateral tracts, cerebellar lesion topography might determine the distribution of
contralateral supratentorial brain tissue changes. We investigated (i) the occurrence of delayed
cerebral atrophy after cerebellar ischemic stroke and its relationship to infarct volume; (ii)
whether cerebellar stroke topography determines supratentorial atrophy location; (iii) how
cortical atrophy after cerebellar stroke impacts clinical outcome.
We performed longitudinal volumetric MRI analysis of patients with isolated
cerebellar stroke from the Swiss Stroke Registry database. Stroke location and volume were
determined at baseline MRI. Delayed cerebral atrophy was measured as supratentorial cortical
volumetric change at follow-up, in contralateral target- as compared to ipsilateral referenceareas. In patients with bilateral stroke, both hemispheres were analyzed separately. We
obtained maps of how cerebellar lesion topography, determines the probability of delayed
atrophy per distinct cerebral lobe. Clinical performance was measured with the National
Institutes of Health Stroke Scale and modified Rankin Scale (mRS).
In 29 patients (age 58±18; 9 females; median follow-up: 6.2 months), with 36 datasets
(7 patients with bilateral cerebellar stroke), delayed cerebral atrophy occurred in 28 (78%)
datasets. A multivariable generalized linear model for a Poisson distribution showed that
infarct volume (milliliter) in bilateral stroke patients was positively associated with the
number of atrophic target areas (Rate ratio=1.08 p=0.01). Lobe-specific cerebral atrophy
related to distinct topographical cerebellar stroke patterns. By ordinal logistic regression (shift
analysis), more atrophic areas predicted higher 3-month mRS scores in patients with low
baseline scores (baseline score 3-5: Odds ratio=1.34; p=0.02; baseline score 0-2: OR=0.71;
p=0.19).
Our results indicate that (i) isolated cerebellar ischemic stroke commonly results in
delayed cerebral atrophy and stroke volume determines the severity of cerebral atrophy in
patients with bilateral stroke; (ii) cerebellar stroke topography affects the location of delayed
cerebral atrophy; (iii) delayed cerebral atrophy negatively impacts clinical outcome.
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