So what the fuck is the solution? I don't care how well you describe the problem, it is totally useless without a solution. Once again more followup needed which will never occur. Maybe some of these might help which your doctor knows nothing about. How fucking incompetent is your doctor and stroke hospital? Don't do these on your own
From June, 2013;
Low Diastolic Pressure Linked to Brain Atrophy
And this from November, 2012:
Relationship between Physical Activity and Brain Atrophy Progression.
And from September, 2014:
Lack of sleep may shrink your brain
From June, 2013:
Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment
Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial
Study shows that IVIG could prevent brain atrophy, delay onset of Alzheimer's disease Oct. 2015
The latest here:
Association between total-Tau and brain atrophy one year after first-ever stroke
- Hege Ihle-HansenEmail author,
- Guri Hagberg,
- Brynjar Fure,
- Bente Thommessen,
- Morten W. Fagerland,
- Anne R. Øksengård,
- Knut Engedal and
- Per Selnes
BMC NeurologyBMC series – open, inclusive and trusted201717:107
DOI: 10.1186/s12883-017-0890-6
© The Author(s). 2017
Received: 31 January 2017
Accepted: 29 May 2017
Published: 5 June 2017
Abstract
Background
Although the most serious
consequence of neuronal ischemia is acute neuronal death, mounting
evidence suggests similarities between stroke and neurodegenerative
disease. Brain atrophy visualized on structural MRI and pathological
cerebrospinal fluid (CSF) concentrations of microtubule-associated
protein tau (T-tau) and phosphorylated microtubule-associated protein
tau indicate neurofibrillary degeneration. We aimed to explore the
association between CSF T-tau and brain atrophy 1 year post-stroke.
Methods
We included 210 patients with
first-ever ischemic stroke or transitory ischemic attack without
pre-existing cognitive impairment. After 12 months, subjects underwent
MRI, and CSF biomarkers were assessed. Using SIENAX (part of FSL),
ventricular CSF volume and total brain volume were estimated and
normalized for subject head size. The association between T-tau as
explanatory variable and ventricular and total brain volume as outcome
variables were studied using linear regression.
Results
One hundred eighty-two
patients completed the follow-up. Forty-four had a lumbar puncture. Of
these, 31 had their MRI with identical scan parameters. Mean age was
70.2 years (SD 11.7). Ventricular volume on MRI was significantly
associated with age, but not with gender. In the multiple regression
model, there was a significant association between T-tau and both
ventricular (beta 0.44, 95% CI 376.3, 394.9, p = 0.021) and global brain volume (beta −0.50, 95% CI −565.9, −78.3, p = 0.011). There was no significant association between CSF T-tau 1 year post-stroke and baseline volumes.
Conclusion
T-tau measured 1 year
post-stroke is associated with measures of brain atrophy. The findings
indicate that acute stroke may enhance or trigger tau-linked
neurodegeneration with loss of neurons.
Trial registration
Clinicaltrials.gov NCT00506818, July 23, 2007.
Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.
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