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.

Tuesday, September 10, 2019

Cilostazol use is associated with FIM cognitive improvement during convalescent rehabilitation in patients with ischemic stroke: a retrospective study

I'm sure your doctor and stroke hospital did absolutely nothing with these 5 earlier posts back to August 2013.  Incompetency in full display right there. Why the hell is stroke in your hospital name when they are doing NOTHING to solve stroke. Ask the board of directors, why they are so fucking incompetent?

 

Cilostazol use is associated with FIM cognitive improvement during convalescent rehabilitation in patients with ischemic stroke: a retrospective study

Joe Senda1,2,3, Keiichi Ito3, Tomomitsu Kotake3, Masahiko Kanamori3, Hideo Kishimoto3,  Izumi Kadono4, Hiroko Nakagawa-Senda5, Kenji Wakai6, Masahisa Katsuno2,  Yoshihiro Nishida4,7, Naoki Ishiguro4,7, and Gen Sobue2,8
1Department of Neurology and Rehabilitation, Komaki City Hospital, Komaki, Japan 2Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan 3Division of Rehabilitation, Kami-iida Rehabilitation Hospital, Nagoya, Japan 4Division of Rehabilitation, Nagoya University Hospital, Nagoya, Japan 5Department of Public Health, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan 6Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan 7Department of Orthopedic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan 8Research Division of Dementia and Neurodegenerative Disease, Nagoya University  Graduate School of Medicine, Nagoya, Japan

ABSTRACT

Cilostazol is a phosphodiesterase III-inhibiting antiplatelet agent that is often used to prevent stroke and peripheral artery disease, and its administration has shown significant improvements for cognitive impairment. We investigate the potential of cilostazol for reducing or restoring cognitive decline during convalescent rehabilitation in patients with non-cardioembolic ischemic stroke. The study sample included 371 consecutive patients with lacunar (n = 44) and atherothrombosis (n = 327) subtypes of non-cardioembolic ischemic stroke (224 men and 147 women; mean age, 72.9 ± 8.1 years) who were required for inpatient convalescent rehabilitation. Their medical records were retrospectively surveyed to identify those who had received cilostazol (n = 101). Patients were grouped based on cilostazol condition, and Functional Independence Measure (FIM) scores (total and motor or cognitive subtest scores) were assessed both at admission and discharge. The gain and efficiency in FIM cognitive scores from admission to discharge were significantly higher in patients who received cilostazol than those who did not (p = 0.047 and p = 0.035, respectively); we found no significant differences in other clinical factors or scores. Multiple linear regression analysis confirmed that cilostazol was a significant factor in FIM cognitive scores at discharge (β = 0.041, B = 0.682, p = 0.045); the two tested dosages were not significantly different (100 mg/day, n = 43; 200 mg/day, n = 58). Cilostazol can potentially improve cognitive function during convalescent rehabilitation of patients with non-cardioembolic ischemic stroke, although another research must be needed to confirm this potential.

No comments:

Post a Comment