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.

Saturday, May 30, 2020

Exercise may prevent hippocampal atrophy in the first year after stroke: Blinded analysis of PISCES pilot data

'May' is not good enough. WE NEED EXACT STROKE PROTOCOLS. GET THERE! If you can do aerobic exercise at two months you are an outlier and this is extreme cherry picking of participants.  Bad research, I blame the mentors and senior researchers on not setting this up properly.  None of this would be able to be extrapolated to the average stroke survivor. No mention of any dropouts being unable to do the exercise.

Exercise may prevent hippocampal atrophy in the first year after stroke: Blinded analysis of PISCES pilot data

Mohamed Salah Khlif1, Emilio Werden1, Laura Bird1, Stanley Hung1, Rosalind Hutchings1, Matthew Pase1, Natalia Egorova1, and Amy Brodtmann1, 2 1 The Florey Institute of Neuroscience and Mental Health, Heidelberg, Victoria, Australia 2 Department of Neurology, Austin Health, Heidelberg, Victoria, Australia
Introduction • Stroke survivors have a high risk of developing cognitive impairment or dementia [1]. • Total and regional brain atrophy precedes such cognitive impairment, especially the reduction in hippocampal volume which is known to be more accelerated in the ipsilateral side to the stroke infarct [2]. • Exercise is a known neuroprotective factor.  We present the preliminary findings comparing total brain volume (TBV) and hippocampal volume (HV) between two stroke groups sampled from the Cognition and Neocortical Volume after Stroke (CANVAS) cohort study [3] and the Post Ischaemic Stroke Cardiovascular Exercise (PISCES) study pilot data [4].

Methods

CANVAS CANVAS is an observational longitudinal study of 135 ischaemic stroke patients and 40 age-matched healthy controls over five years. Stroke patients were recruited from the Acute Stroke Units of the Austin, Box Hill, and Royal Melbourne, hospitals in Victoria, Australia. Inclusion criteria included age over 18 years, ischaemic stroke of any type confirmed on clinical imaging, and no history of dementia or any other neurodegenerative condition. Ethical approval was granted by each hospital’s Human Research Ethics Committee.
PISCES
PISCES is a Phase-2b randomised controlled trial investigating the effects of aerobic exercise on brain volume and cognitive function after ischaemic stroke. Patients who have suffered an ischaemic stroke are enrolled in one of two 8-week exercise programmes, beginning at two months post-stroke. The exercise programme involves either combined aerobic exercise and resistance training (intervention group) or balance and stretching (control group). Cognitive function and brain volumes are assessed at two, four, and 12 months post-stroke.
MRI acquisition T1-weighted MPRAGE sequences were obtained using 3T Siemens scanner (Siemens, Erlangen, Germany): 160 slices; repetition time, TR = 1900 ms; echo time, TE = 2.6 ms; inversion time, TI = 900 ms; flip angle = 9°; field of view: 256 × 256 pixels; voxel size = 1 mm3.
MRI segmentation We used the longitudinal pipeline [5] in FreeSurfer v6.0 to estimate total brain volume (TBV) and hippocampal volume (HV) in 125 CANVAS and 16 PISCES participants at two and 12 months post-stroke.
Statistical analysis We used repeated measures ANOVA (fitrm, ranova, and multcompare in MATLAB 2018a) to estimate volumetric changes between time points. Age, sex, years-ofeducation, and total intracranial volume (TIV) were used as covariates.

Results

Demographic characteristics There was no statistical difference in age, sex, education level, or TIV between the CANVAS and PISCES stroke groups.
Covariates Age, education, and TIV were associated with TBV and HV; sex was not.
Total brain volume • TBV was numerically, but not significantly, higher in the PISCES group at both time points (see Fig. 1). • There were no significant reductions in TBV between time points (PISCES: 2.16%, p = 0.079; CANVAS: 0.69%, p = 0.15).
Hippocampal volume • Contralesionally, HV was reduced by 0.26% (p = 0.62) in the PISCES group and 0.66% (p = 0.0007) in the CANVAS group. • Ipsilesionally, HV was also significantly reduced between time points for CANVAS (1.47%, p = 0.002). However, for PISCES, HV has increased by 2.15%, though not significant (p = 0.10).
Figure 1: TBV and HV at two and 12-month time points (volumes are in mm3, error bars = standard error)

Conclusions 

In this small pilot PISCES sample, we observed a trend for reduced hippocampal atrophy in our stroke group. These data are still blinded (both exercise programs were analysed as one group), but the exercise interventions may have played a role in the reduction of hippocampal atrophy on the contralesional side, while possibly leading to hippocampal neurogenesis on the ipsilesional side

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