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.

Saturday, November 5, 2011

The influence of positioning upon cerebral oxygenation after acute stroke: a pilot study

So who has followed up on this to see how best to position a patient after a stroke? Or does it not matter because we should first be figuring out how to open the capillaries that are closed by pericytes?
http://ageing.oxfordjournals.org/content/37/5/581.full
Passive postural changes may have an effect on a number of physiological parameters after stroke [1]. For example, standing, sitting or even elevating the head after stroke might reduce cerebral blood flow due to poor collateral circulation and an inability to regulate and augment cerebral blood flow in ischaemic regions of the brain [2–5]. Optimal positioning for patients in the acute stage after stroke is still unknown [6–8]. Variation in clinical practice is evident in the literature [5–9] and has been observed [10]. This variation could be because of the paucity of experimental findings to inform a scientific rationale for positioning early after stroke. For example, traditionally, people who have suffered a large hemispheric stroke have been managed with head elevation between 30° and 45° [5], a practice generalised from clinical experience with head trauma patients despite differences in pathophysiology [11].
There is some experimental evidence that positional change may alter cerebral haemodynamics after stroke [12, 13]; but, there is disagreement on how this is changed early after the ictus [12–15]. Moreover, the natural history of autoregulation following stroke is unclear [16]. At present, there is a paucity of evidence to support or refute the possibility that in some people the vulnerable ischaemic penumbra might be at risk from a reduction in cerebral blood flow mediated through positional changes after stroke [1].
To be relevant clinically, cerebral oxygenation needs to be measured in relation to changes in posture. It also needs to be measured in real time at the bedside to enable appropriate clinical decisions about positioning. The relatively new technology of near infrared spectroscopy (NIRS), a minimally invasive technique, offers the possibility of making such measurements [17]. The aim of this pilot study is to explore whether changes in position, involving different placements of the head and upper body in relation to gravity, in the first week after a middle cerebral artery cortical ischaemic stroke produce changes in cerebral oxygenation in the region of the arterial territory.

Methods

A replicated single case study design was used with the phase sequence ABACA (details in procedure section below). The study was approved by the Local Research Ethics Committee and participants provided either written informed consent or, if that was not possible, assent was provided by their next-of-kin.
Participants were adults who had suffered a middle cerebral artery cortical ischaemic stroke, confirmed by computer tomography (CT) no more than 7 days prior to testing. Exclusion criteria were: a previous stroke in the same division of the ipsilesional medial cerebral artery (MCA) territory; critical illness (peripheral oxygen saturations <90% on air, pulse >100 beats per min, systolic BP <90 mmHg, Glasgow Coma Score <10); inability to follow one-stage command; and, inability to sit upright on the edge of a bed with support from one person.
Participants were seated in a multi-position chair (see instrumentation below) in a quiet room adjacent to the acute stroke unit. Two optodes were placed bihemispherically on their scalp with a 4 or 5 cm distance between the receiving and emitting probes over each hemisphere. Positional accuracy of the optodes was achieved through superficial scalp marking over the ischaemic lesion using laser guidance at CT scanning and mirrored over the opposite hemisphere. An electronic topical recorder was used to record peripheral oxygen saturations, pulse and blood pressure at 2-min intervals. This ensured systematic haemodynamic changes were demonstrated independently of cerebral monitoring. Each participant then completed the standardised five-phase posture sequence designed to reproduce positions often used during the first week after stroke:
  • A phase—supine lying.
  • B phase −45° back-rest/seat with legs raised up straight as if lying propped up in bed.
  • A phase—supine lying.
  • C phase—sitting upright with hips, knees and ankles at 90° as if sitting in a chair.
  • A phase—supine lying.
After an initialisation phase of 15 min supine, each postural challenge lasted up to15 min depending upon subjects' comfort in the position.
A two-channel ‘NIRO 300’ (Hamamatsu Photonics K.K. Japan) was used to record data on cerebral oxygenation at 2 Hz. The ‘NIRO 300’ produces infra-red light via an emitting probe which directs the photons perpendicular to the tissue surface. A receiving probe detects the incident and transmitted light intensities from the tissue. Inbuilt computational software utilising algorithms generated from the modified Beer–Lambert law display and record relative changes in the concentration of oxygenated haemoglobin (Δ[HbO2]), deoxygenated haemoglobin (Δ[Hb]) and oxidised cytochrome oxidase (Δ[CtOx] ) over the period of study. Using the technique of spatially resolved spectroscopy (SPS), a measure of absolute tissue oxygen saturation, the tissue oxygenation index (TOI) can be generated. TOI is the ratio of oxygenated ([HbO2]) to total tissue haemoglobin concentrations ([HbT]) [17].
The multi-position chair used for testing had an adjustable back- and leg-rest enabling any position between lying supine and sitting with hips, knees and ankles at 90°. Position was controlled by the researcher through a hand-held electronic device.
The descriptive data collected for participants were: age, gender and the National Institute of Health Stroke Scale (NIHSS) [18].
The primary outcome was bihemispheric NIRS monitored TOI (i.e. the ratio of oxygenated ([HbO2]) to total tissue HbT.
The probability of serial dependency in 1-min sets of data, collected immediately before and after each posture change, was tested using the autocorrelation coefficient and Bartlett's test. All data sets were significantly autocorrelated-r > 0.183, range 0.285–0.991. Statistical comparison of phases was therefore invalid and data were plotted and then interpreted by visual inspection for trend and level.

Results

Seven people who met the study criteria were included. In summary, their mean age was 70.71 years (range 58–81 years); five were male and the median time for measurement after stroke was 5 days (range 4–7). Subject characteristics are presented in Appendix 1 in the supplementary data on the journal's website. Two patients (subjects 2 and 3) had their anti-hypertensive medication continued after stroke onset and one patient (subject 2) had occlusion of the ipsilateral internal carotid artery. One patient (subject 2) exhibited orthostatic hypotension (defined as a drop in systolic blood pressure ≥20 mmHg) on postural challenges. There were no changes noted in heart rate or oxygen saturations.
Visual inspection of the plotted data indicated that six of the seven patients (subjects 1, 2, 3, 5, 6, 7) demonstrated changes in TOI between supine and sitting up positions. In these patients, the pattern displayed a maximum value of TOI in the supine position and a reduction of TOI on sitting up in the affected middle cerebral artery territory (Figures 1 and 2). There were also similar changes in TOI observed in the contra-lateral lobe (subjects 1, 2, 3, 6, 7); but these were less marked. In one patient (subject 5), TOI was maximal in the upright position and reduced in the supine position in the contra-lateral lobe only.

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