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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, May 29, 2014

Current Perspectives in Post-stroke Cognitive Impairment

I couldn't make head or tails of what possible stroke protocols could come from this. Ask your doctor. Go to bottom for one highlighted line which is distressing, I've been using a 33% dementia chance from an Australian study.
http://www.touchneurology.com/articles/current-perspectives-post-stroke-cognitive-impairment
This article summarises the content of a symposium that took place during the 21st World Congress of Neurology in Vienna, Austria. It aims to describe the vascular and cellular processes that are involved in the maintenance of the blood–brain barrier (BBB), the cells involved in the neurovascular unit (NVU) and its dysfunction in stroke resulting in poststroke cognitive impairment (PSCI) for many patients. There is substantial variability in eported rates of PSCI and this is largely a result of differing assessment methods used to assess the condition and inconsistent treatments and times to treatment initiation in different territories. The lack of agreed guidelines and of consensus among healthcare professionals also contributes to variable levels of diagnosis and treatment outcomes in PSCI. This article will additionally consider these critical matters and discuss the development of a new treatment approach for PSCI that has shown potential and is being evaluated in clinical trials.

The Role of the Blood–Brain Barrier and the Neurovascular Unit in Cerebral Ischaemia An important concept in the development of stroke and consequent cognitive impairment is the fact that the brain has no reserve of energy or oxygen. It must therefore be constantly perfused through the normal blood supply to supply these factors and to remove metabolic products, particularly carbon dioxide. Any interruption in this continuous process is liable to have a serious effect on the brain region in which it occurs.1The BBB comprises a diverse set of cellular components some of which participate in the NVU. The interaction between these cells is important in the pathophysiology of PSCI and other neurological diseases (see Figure 1).2–4

The tissues of the central nervous system (CNS) make high metabolic demands of the vascular system and the microcirculation of the brain must be responsive to changing requirements.5,6 The NVU is central to this process and maintains a ‘metabolic coupling’ between brain activity and blood flow. In neurological disease or injury there is a danger of exposure to metabolic products that are toxic to brain tissue and may cause neuronal damage.4,7 ATP-sensitive potassium channels play a major role in sensing metabolic requirements and provide protection of brain tissues against these effects of neurological disease or injury.8 Some functional magnetic resonance imaging (fMRI) studies have suggested that following stroke there is an uncoupling between metabolic requirements, especially for oxygen and vascular supply and this can worsen outcomes.9

Within the NVU, astrocytes provide trophic support to neurons and maintain synaptic functions and dynamic signalling. The end-feet structures of astrocytes have a close contact with cerebral endothelial cells and provide a physical link to the microvasculature. Astrocytes are therefore uniquely positioned to exercise control over local changes in cerebral blood flow as well as regulating tight junction integrity.1,10,11 Pericytes are important in regulating blood flow by contracting or relaxing in response to vasoactive stimuli from surrounding cells.12,13

Microglial cells are cerebral monocytes with a stellate morphology and release a range of pro- and anti-inflammatory mediators but their role in the NVU is as yet, unclear.14–16 In response to changes in neuronal activity, perivascular-released neurotransmitters and other mediators can activate receptors on both smooth muscle cells and astrocytes to alter the tone of brain microvessels.17

Cellular communication within the NVU involves various signalling pathways of neurovascular coupling and interactions among astrocyte, vascular smooth muscle, neuronal and endothelial compartments. These processes comprise numerous factors including cytochrome P450 epoxygenase metabolites, signalling initiated by metabotropic glutamate receptor (mGluR) activation, potassium signalling, 20-hydroxyeicosatetraenoic acid (20-HETE acid) signalling, adenosine signalling, carbon monoxide signalling and calcium (Ca2+) efflux. In addition, the regulation of blood flow by astrocytes may involve both vasodilating and vasoconstricting components.18

Several neurotransmitters are important in vascular coupling in the NVU. Glutamate is the main excitatory neurotransmitter in the brain and may trigger responses via indirect signalling.19 The release of glutamate during neuronal activation may act on astrocytic mGluR receptors to increase Ca2+ in astrocytes and elicit a vasodilatory effect.20 Nitric oxide is released from activated neurons following N-methyl-D-aspartate (NMDA) receptor activation21 and is one of the major vasoactive substances whose role is of prime importance in maintaining endothelial homeostasis. Calcium waves are another form of neurotransmitters and are a type of non-electrical impulse in which increased blood flow results in greater intracellular Ca2+ concentrations in astrocytes and the signal is propagated by release of Ca2+ to surrounding cells or by extracellular ATP signalling.22

The variability of post-stroke cognition assessment methods is highlighted by the finding that in patients with MCI (without dementia) 3 months after a stroke varies from 17–66 % depending on the criteria used for testing.33 

4 more pages and references at link.

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