Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, December 16, 2021

Delayed cerebral atrophy after cerebellar stroke: topographical relation and clinical impact

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 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 © 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. Downloaded from https://academic.oup.com/braincomms/advance-article/doi/10.1093/braincomms/fcab279/6437996 by guest on 30 November 2021 

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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