Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Wednesday, June 21, 2017

Anti-anxiety medications change the brain

With a 28% rate of generalized anxiety disorder in stroke survivors your doctor should have a protocol to address that.   You probably need to challenge your doctor if Benzodiazepines are suggested as a solution, but I know nothing since I am not medically trained.
Benzodiazepines—the family of popular sedatives that includes Valium and Xanax—seem to bring about structural changes in the brain, according to a European study running in the August edition of Psychiatry Neuroimaging.
Sanna Huhtaniska, MD, of the University of Oulu in Finland and colleagues describe their work assessing brain MRI scans from 38 persons with schizophrenia at 34 years old and then again at 43 years old.
Stating their belief that theirs is the first neuroimaging study to home in on “benzos” in the brain, the authors report they found that higher long-term benzodiazepine use associated with reductions in the volume of the caudate. This held even after adjusting for illness symptom scores and cumulative use of antipsychotic medications.
The team also found that, when taking into account illness severity measures and benzodiazepine dose, higher long-term use of antipsychotic meds was associated with increases in lateral ventricular volume.
The authors acknowledge that their work focused on a small sample and did not take into account numerous possible confounding factors such as alcohol use, physical activity levels and nonpharmacological interventions.
They cite as strengths their use of comprehensive, thoroughly collected medication data—they drew from the general-population Northern Finland Birth Cohort 1966 study—and their subjects’ accessing of clinical services in naturalistic rather than research settings.
Huhtaniska and team urge caution in interpreting their findings. The ventricular enlargement they observed in association with antipsychotic medications “may be a marker for a factor we are unable to identify,” they write.
Meanwhile, their finding of caudate reduction associated with cumulative benzodiazepine medication necessitates more studies, they state.
“There is a need for understanding the mechanisms behind antipsychotic- and benzodiazepine-related structural and functional changes in the brain,” the authors write. “Further studies should also focus on how medication-related structural alterations correspond to cognition and functioning.”

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