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

Monday, March 13, 2017

Anatomical Parameters of tDCS to Modulate the Motor System after Stroke: A Review

I saw nothing in here that said what the objective diagnosis would need to be to have this become useful for an intervention. But then no protocol was mentioned either. So this whole fucking article was useless.
http://journal.frontiersin.org/article/10.3389/fneur.2017.00029/full?

Variability and Lack of Reliability of tDCS Studies in Individuals with Stroke

The variable effects of tDCS on motor performance may be due to the lack of standardization of the technical parameters used across sites. More likely, however, it is also due to (1) the heterogeneity of the populations involved in the studies (43) and (2) the variability of the motor paradigms used.

Heterogeneity of the Involved Populations

The heterogeneity of each study population is a potential source of variability for tDCS effects. However, researchers have had difficulty in finding consistent sources of variability. Studies typically examine the effects of (1) individual biological variability (e.g., metabolic/genetic variants), or, factors specific to the stroke such as, (2) time since stroke, (3) the nature and location of the stroke, and finally (4) the level of motor impairment.

Individual Biological Variability

Intrinsic individual differences in neurotransmitter levels, metabolic factors, and genetic variants provide a complex source of variability when it comes to tDCS responsiveness. For instance, one study found a relationship between individual differences in baseline measures of GABA and anodal stimulation outcomes. However, this relationship was not found between GABA and cathodal or bi-hemispheric stimulation outcomes (46). Another study showed that individual differences in the level of dopamine receptor (D1) activity influenced the excitatory effects of anodal tDCS on M1 (47). These studies suggest that there is a complex, but influential, relationship between biological factors and stimulation response.
Another factor that has been widely explored is the role of an individual’s genetic variability on tDCS response. The secretion of brain-derived neurotrophic factor (BDNF), which is involved in the synaptic plasticity, neuronal growth, long-term potentiation (LTP) formation, and long-term memory storage (4850), seems to be enhanced by the application of tDCS (51). Moreover, an individuals’ level of BDNF seems to influence the response to NIBS and especially to tDCS (28, 52). The most common form of BDNF polymorphisms, in which an amino acid substitution between a Valine and a Methionine at position 66 on the BDNF gene [Val66Met (53)], modulate the level of BDNF expression and are thus associated with a differential modulation of brain plasticity and altered motor plasticity (54). The Val66Met polymorphism, which induces less BDNF expression, has also been shown to be associated with less-efficient motor learning and reduced responsiveness to all forms of NIBS (28, 54, 55).
However, this finding is not always consistent. For example, one study did not find any impact of the BDNF polymorphism on the neuroplastic changes induced by anodal tDCS in older adults (56), while a second one failed to find any impact of the BDNF polymorphism on the neuroplastic-induced changes associated with either tDCS, transcranial random noise stimulation, or theta burst stimulation (57). Another study demonstrated that the BDNF polymorphism did not predict responses to tDCS in patients suffering from depression but that a serotonin transporter polymorphism did (58). This suggests that the impact of the BDNF polymorphism, or more globally, genetic polymorphisms on NIBS-related effects, may be disease or task dependent.

Time after Stroke

There are also a number of factors specific to individuals with stroke that may affect stimulation efficacy. One variable is that stimulation may be delivered at different times after stroke, during which different neural plasticity mechanisms (59, 60) are active, making it difficult to compare effects across time points. In addition, the categorical definitions of “time after stroke” may be variable as well. For instance, the “chronic phase” of stroke is defined across studies as patients anywhere from 3 months or more (up to many years) after stroke (61, 62). This means that within one “category” of patients with stroke, there may be enormous variability in the plasticity processes and thus the potential tDCS effects and interactions with those processes. More precise clarification of time after stroke, using absolute terms such as months, may be useful for comparing post-stroke tDCS results.

Nature and Location of the Stroke

The location of the stroke lesion (i.e., cortical or subcortical lesion) is similarly mixed or omitted in some tDCS studies (61, 6366). However, neural plasticity processes and cortical reorganization inducing differential recruitment of different brain regions may be dependent of the size and location of the stroke (67). Another source of stroke-specific variability is the nature of the stroke (i.e., ischemic or hemorrhagic), with some studies mixing both populations together (18, 65, 66, 68). This could also be a potential confound as the deficits and brain plasticity processes associated with cortical/subcortical localization or ischemic or hemorrhagic stroke (6971) could be different.

Level of Motor Impairment after Stroke

Finally, the level of impairment after stroke should be carefully considered. There is a wealth of literature that suggests that patterns of neural recovery may differ for individuals based on the severity of their stroke (7276). The recruitment of different brain regions, such as the contralesional hemisphere, may also play a different role based on the level of motor impairment. Most of the tDCS studies in patients after stroke mixed patients with different level of impairments (from mild to severe) (18, 65, 77). However, it may be important to consider an individual’s level of motor impairment and optimal pattern of recovery when applying tDCS.

More at link.

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