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.

Showing posts with label research objective. Show all posts
Showing posts with label research objective. Show all posts

Tuesday, June 4, 2019

Quality of life and disability after severe stroke and early neurological rehabilitation

Pretty much useless, there was no objective analysis of the starting point and the therapy delivered to the results achieved.  ISN'T THAT THE WHOLE FUCKING POINT OF STROKE THERAPY? WHAT WORKS AND WHAT DOESN'T? The mentors and senior researchers involved in this need to be fired.

Quality of life and disability after severe stroke and early neurological rehabilitation

Abstract

BACKGROUND: Data on the long-term effects on quality of life of patients after severe stroke and discharge from early institutional rehabilitation are important for guiding the early rehabilitation phase and the further outpatient care.
OBJECTIVE: Analysis of the outcome of patients following severe stroke 3 and 12 months after discharge from early neurological rehabilitation.(What the fuck stupid objective is this? It should be; What interventions provide the best outcomes.)
METHODS: Analysis of the Asklepios Hamburg multicenter early stroke rehabilitation registry (ICD 10: I61, I60, I63 and OPS 8‑552). Structured interviews with documentation of disabilities using the early rehabilitation Barthel index (ERBI), modified Rankin scale (mRS) and quality of life (12-item short form health survey, SF-12). Assessment of further treatment and complications 3 and 12 months after discharge from the early rehabilitation departments by telephone interviews. RESULTS: Out of 1045 treated stroke patients 270 were enrolled between October 2015 and November 2017 and 200 and 151 patients could be followed up after 3 and 12 months, respectively. There was a significant improvement (p < 0.001) in the median ERBI (151 patients at 12 months). Factors influencing a poorer functional outcome (higher mRS) at 12 months were a higher mRS at discharge (OR 5.43 [1.18, 25.09], p = 0.03) and age (per decade OR 1.5 [1.09, 2.02]; p = 0.01). Female sex reduced the risk for a poorer outcome after 12 months (OR 0.49 [0.25, 0.96]; p = 0.04). Quality of life (SF-12) was not different over time. The mental quality of life showed no differences (p = 0.32) compared to a historical, significantly less (p<0.001) handicapped stroke collective.
CONCLUSION: The surviving severe stroke patients recovered significantly up to 12 months after discharge. The mental quality of life did not differ from that of a historical less handicapped collective.(Then you didn't ask the right questions, with the caregiver not present. You browbeat them into accepting your tyranny of low expectations.)

Wednesday, February 13, 2019

The Influence of Primary Motor Cortex Inhibition on Upper Limb Impairment and Function in Chronic Stroke: A Multimodal Study

So the objective had nothing to do with getting survivors recovered. Not even barely tangentially.

The Influence of Primary Motor Cortex Inhibition on Upper Limb Impairment and Function in Chronic Stroke: A Multimodal Study

First Published February 11, 2019 Research Article
Background. Stroke is a leading cause of adult disability owing largely to motor impairment and loss of function. After stroke, there may be abnormalities in γ-aminobutyric acid (GABA)-mediated inhibitory function within primary motor cortex (M1), which may have implications for residual motor impairment and the potential for functional improvements at the chronic stage.
Objective. To quantify GABA neurotransmission and concentration within ipsilesional and contralesional M1 and determine if they relate to upper limb impairment and function at the chronic stage of stroke.  
Methods. Twelve chronic stroke patients and 16 age-similar controls were recruited for the study. Upper limb impairment and function were assessed with the Fugl-Meyer Upper Extremity Scale and Action Research Arm Test. Threshold tracking paired-pulse transcranial magnetic stimulation protocols were used to examine short- and long-interval intracortical inhibition and late cortical disinhibition. Magnetic resonance spectroscopy was used to evaluate GABA concentration.
Results. Short-interval intracortical inhibition was similar between patients and controls (P = .10). Long-interval intracortical inhibition was greater in ipsilesional M1 compared with controls (P < .001). Patients who did not exhibit late cortical disinhibition in ipsilesional M1 were those with greater upper limb impairment and worse function (P = .002 and P = .017). GABA concentration was lower within ipsilesional (P = .009) and contralesional (P = .021) M1 compared with controls, resulting in an elevated excitation-inhibition ratio for patients.
Conclusion. These findings indicate that ipsilesional and contralesional M1 GABAergic inhibition are altered in this small cohort of chronic stroke patients. Further study is warranted to determine how M1 inhibitory networks might be targeted to improve motor function.