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:

Saturday, September 3, 2016

Enhanced apoptosis from early physical exercise rehabilitation following ischemic stroke

They talked around and around the question and as far as I can tell never clearly answered the question. 'When should exercise start?' Enhanced sounds like such a positive word but in this context is not.The drumbeat around the stroke medical world is that the earlier rehab starts the better.

Efficacy and safety of very early mobilisation within 24 h of stroke onset (AVERT): a randomised controlled trial

Early exercise improves cerebral blood flow through increased angiogenesis in experimental stroke rat model

Early Mobilisation Following Stroke



 So what is the fucking time to start rehab?

Enhanced apoptosis from early physical exercise rehabilitation following ischemic stroke

  • SIGNIFICANCE The use of exercise-mediated adaptations to attenuate physical disability after stroke is an emerging arena in neurotherapeutics. However, fundamental questions regarding initiation time, which affect rehabilitation, remain unanswered. Although current guidelines recommend starting out-of-bed activity “early” during the acute phase of care, such guidelines do not specify how early exercise optimizes outcome. Our results shed light on the time-sensitive effect of exercise in poststroke rehabilitation.


The effectiveness of the rehabilitative benefits of physical exercise appears to be contingent upon when the exercise is initiated after stroke. The present study assessed the hypothesis that very early exercise increases the extent of apoptotic cell death via increased expression of proapoptotic proteins in a rat stroke model. Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 hr using an intraluminal filament and assigned to four nonexercise and three exercise groups. Exercise on a Rota-Rod was initiated for 30 min at 6 hr (considered very early), at 24 hr (early), and at 3 days (relatively late) after reperfusion. At 24 hr after exercise, apoptotic cell death was determined. At 3 and 24 hr after exercise, the expression of pro- and antiapoptotic proteins was evaluated through Western blotting. As expected, ischemic stroke significantly increased the levels of apoptotic cell death. Compared with the stroke group without exercise, apoptotic cell death was further increased (P < 0.05) at 6 hr but not at 24 hr or 3 days with exercise. This exacerbated cell injury was associated with increased expression of proapoptotic proteins (BAX and caspase-3). The expression of Bcl-2, an antiapoptotic protein, was not affected by exercise. In ischemic stroke, apoptotic cell death was enhanced by very early exercise in association with increased expression of proapoptotic proteins. These results shed light on the time-sensitive effect of exercise in poststroke rehabilitation. © 2016 Wiley Periodicals, Inc.
Postinjury exercise therapy that aims to ameliorate physical disability after stroke has long been considered a logical candidate for neuroprotective rehabilitation (Arya et al., 2011). In previous studies, neuroprotection has been consistently evidenced by physical exercise through reduced sequelae of brain infarction with improved functional outcomes in a rat ischemic stroke model (Ding et al., 2006; Dornbos et al., 2013; Q.W. Zhang et al., 2013). With experimental animal models of stroke, some studies have suggested a beneficial effect of exercise initiated as early as 24 hr after the onset of ischemic or hemorrhagic stroke (Park et al., 2010; Matsuda et al., 2011; P. Zhang et al., 2013). Furthermore, only mild to moderate but not heavy exercise, if initiated early, is thought to promote recovery from ischemic stroke in rats (Lee et al., 2009). In contrast, training initiated 24 hr after permanent focal brain ischemia was found to exacerbate cortical tissue loss (Humm et al., 1998; Risedal et al., 1999). Furthermore, increased injury was detected in the forelimb area within the sensorimotor cortex of rats that were forced to overuse the impaired forelimb for 7 or 15 days postischemic stroke (Kozlowski et al., 1996; Humm et al., 1998). Together these studies highlight the importance of exercise timing poststroke with regard to recovery from injury and physical disability.
The molecular underpinnings of apoptotic cell death following cerebral ischemia are well established. During periods of reduced oxygen delivery, proapoptotic proteins, such as caspase-3 and BAX, become upregulated and are one of the major causes of neuronal death during ischemia/reperfusion injury (Wu et al., 2003). Conversely, Bcl-2 is an antiapoptotic protein that plays a critical role in cellular survival by acting as a repressor of apoptosis (Korsmeyer, 1995). Thus, the aim of the present study was to determine the effect of physical exercise therapy on apoptotic cell death and the expression of associated pro- and antiapoptotic proteins. We directly compared the effect of poststroke exercise on brain injury at 6 hr, 24 hr, and 3 days after reperfusion with the corresponding nonexercise group. Following a 2-hr middle cerebral artery occlusion (MCAO), we evaluated the extent of apoptotic cell death and the expression of proapoptotic (caspase-3 and BAX) and antiapoptotic (Bcl-2) protein

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