6 Ways Alcohol Can Be Unexpectedly Good For Your Mind And Brain

I think I covered most of these already, but you probably need the research support to counteract your doctors reflexive prohibition against all alcohol.
Mine are here:

Alcohol for these 12 reasons.  

They did miss the extremely important one for survivors. The extra balance training you get will make that part of recovery so much faster - don't do this.
http://www.spring.org.uk/2016/01/6-ways-alcohol-can-be-unexpectedly-good-for-your-mind-and-brain.php?

1. Better cognitive function

Moderate consumption of wine is linked to higher performance on cognitive tests, research has found.

2. You look more attractive

One or two glasses of wine can make the drinker look more attractive to others, a new study finds.
Three or four glasses, though, does not make a person look more attractive than when they are sober.

This is different to the ‘beer goggles’ effect, which is well known: that alcohol makes other people look more attractive.

3. Lower Alzheimer’s risk

One drink a day (or less) for women and 1-2 drinks (or less) for men reduces the risk of developing dementia, a study has found.

4. Lower risk of depression

Wine drunk in moderation can reduce the risk of developing depression, research finds.

5. Better memory for the past

For people over 60, light or moderate alcohol intake is associated with better recall of past events, according to a recent study.

6. Improved spatial memory

One to three glasses of champagne each week could slow memory loss from ageing, recent research finds.

Is Axon Guidance by Attraction and Repulsion, or by a Roll of the Dice?

When your axons are trying to find their way around damaged areas. Which stroke protocol is your doctor using? Attraction? or Repulsion?
I'd be willing to bet a lot of money that your doctor has no f*cking clue about this subject. 
http://wadsworthguidance.blogspot.com/2014/10/is-axon-guidance-by-attraction-and.html
Just a hint of some of the goodies your doctor needs to know about.

direction, X	probability
ventral	P(X = ventral)
anterior	P(X = ventral)
posterior	P(X = ventral)
dorsal	P(X = ventral)

  

In general, the probability distribution of variable X, the direction of outgrowth, is

It satisfies the following condition:
 
This just says that if all the probabilities for all the possible directions are added together the sum must equal 1.  
This little bit of probability theory is simple, but has profound implications.  It means that a guidance cue must affect the probability of outgrowth in more than one direction.  Since the sum of all the probabilities must equal 1, if a cue increases or decreases the probability of outgrowth in one direction it must alter the probability of outgrowth in another direction(s) as well.

 

CXCL12 N-terminal end is sufficient to induce chemotaxis and proliferation of neural stem/progenitor cells

I didn't understand so ask your doctor to translate and put into a useful stroke protocol. Unless you ask, nothing is going to get done.
http://www.sciencedirect.com/science/article/pii/S1873506113000767

Abstract

Neural stem/progenitor cells (NSC) respond to injury after brain injuries secreting IL-1, IL-6, TNF-α, IL-4 and IL-10, as well as chemokines members of the CC and CXC ligand families. CXCL12 is one of the chemokines secreted at an injury site and is known to attract NSC-derived neuroblasts, cells that express CXCL12 receptor, CXCR4. Activation of CXCR4 by CXCL12 depends on two domains located at the N-terminal of the chemokine. In the present work we aimed to investigate if the N-terminal end of CXCL12, where CXCR4 binding and activation domains are located, was sufficient to induce NSC-derived neuroblast chemotaxis. Our data show that a synthetic peptide analogous to the first 21 amino acids of the N-terminal end of CXCL12, named PepC-C (KPVSLSYRCPCRFFESHIARA), is able to promote chemotaxis of neuroblasts in vivo, and stimulate chemotaxis and proliferation of CXCR4 + cells in vitro, without affecting NSC fate. We also show that PepC-C upregulates CXCL12 expression in vivo and in vitro. We suggest the N-terminal end of CXCL12 is responsible for a positive feedback loop to maintain a gradient of CXCL12 that attracts neuroblasts from the subventricular zone into an injury site.