But your doctor will know how to apply this to your stroke protocol.
But the first line is depressing.
http://www.sciencedirect.com/science/article/pii/S0006899305004014
Abstract
Both
increased and decreased testosterone levels have been reported to
correlate with poor outcome after acute ischemic stroke. The present
study focused on the role of testosterone during recovery from
neurological deficits in a rat focal ischemia model. Castrate male rats
were subjected to behavioral tests after 90 min of middle cerebral
artery occlusion (MCAO). On day 7 post-MCAO, neurological
deficit-matched rats were assigned to a treatment group implanted with
subcutaneous testosterone pellets or a control group implanted with sham
cholesterol pellets. After 4 weeks post-MCAO, the average infarct
volume was not significantly different between the two groups. Rats in
the testosterone group demonstrated significantly earlier improvement in
neurological deficits and shortened latency of adhesive tape removal
compared with the control group as analyzed by Wilcoxon signed ranks
test. Walking on parallel bars improved in both groups with a trend
towards early recovery observed in the testosterone group. Biased left
body swings persisted during the test period in both groups post-MCAO.
Serum testosterone was within physiological levels in the treatment
group but was not detectable in the control group by radioimmunoassay.
GAP-43 and synaptophysin expression did not differ between groups. Less
GFAP expression and reactive astrocyte hypertrophy were found around the
infarct area in testosterone-treated rats compared with control rats.
In conclusion, testosterone replacement post-MCAO accelerated functional
recovery in castrate rats, suggesting a potential therapeutic role for
testosterone replacement in stroke recovery.
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