Speed, Ecstasy Accelerate Heart Aging

Maybe  you want to accelerate aging  in order to recover from your stroke. But ask your doctor for details. I know nuthin.

Can ecstasy treat the agony of PTSD?

‘Ecstasy’ as a social drug: MDMA preferentially affects responses to emotional stimuli with social content

Study reveals how ecstasy acts on the brain and hints at therapeutic uses

A ‘Party Drug’ May Help the Brain Cope With Trauma - Ecstasy

 

 

 

http://www.medpagetoday.com/PublicHealthPolicy/PublicHealth/63049?

• by Nicole Lou
  Contributing Writer, MedPage Today February 09, 2017
• This article is a collaboration between MedPage Today® and:
  

Abuse of amphetamines was associated with premature biological aging in a way that was more aggressive than tobacco smoking, according to a single-center study.
After adjusting for multiple variables, amphetamine users had prematurely aging hearts as measured by arterial stiffness (P<0.0001), according to the study published online in Heart Asia.
And the biological age-to-chronological age slope was steeper with amphetamines than among tobacco user, Albert Stuart Reece, MD, and colleagues of the University of Western Australia, and colleagues reported.
"The process seems to occur more aggressively than with tobacco smoking," they wrote. "It appears to follow a different time course to that of the positive methadone control group."
"The implication from the present work is that recurrent habitual amphetamine abuse ages the cardiovasculature, and likely the whole organism generally. It is therefore conceivable that stimulant abusers do physiological and cardiovascular harm," they suggested.
Most (94%) users used amphetamines such as "speed," "ice," and "ecstasy" in the previous week; almost half (47%) reported use the day prior.
"These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment," Reece's group wrote, although they admitted that they lacked dosage data.
Accelerated aging declined with time since last amphetamine use.
Asked by MedPage Today to provide comment, Matthias Liechti, MD, MAS, of University of Basel in Switzerland, argued that this shows that at least part of the "so-called aging" is simply vasoconstriction.
"Although chronic amphetamine use seems unlikely to benefit the circulation, I am not convinced that these changes are chronically lasting -- at least not the ones shown in this study," he wrote in an email.
Reece and colleagues included 713 patients in their study: 55 amphetamine users, 107 tobacco smokers, 483 non-smokers, and 68 methadone patients. The investigators measured heart age by radial arterial pulse tonometry (the SphygmoCor monitoring system).
Liechti questioned whether it was possible to control for all the lifestyle and health factors associated with amphetamine use, such as tobacco smoking. "In a between-subject study, such as the present one, it is difficult to control for these factors. So the changes in the vasculature, if at all of a lasting nature, may rather be linked to factors associated with amphetamine use disorder rather than reflect a lasting problem of the substance itself."
"Also note, that ADHD children use amphetamine daily and for years and they do not seem to suffer from any vascular problems," he added.
He conceded that the same cannot be said confidently for d-amphetamine and mixed amphetamines, however.

Reece and Liechti declared no conflicts of interest.

last updated 02.14.2017

• Primary Source

  Heart Asia

  Source Reference: Reece AS, et al "Acceleration of cardiovascular-biological age by amphetamine exposure is a power function of chronological age" Heart Asia 2017; DOI: 10.1136/heartasia-2016-010832.

Reperfusion Beyond 6 Hours Reduces Infarct Probability in Moderately Ischemic Brain Tissue

So from this could we calculate the death rate of neurons during the week or so that the neuronal cascade of death is occurring? We never will solve that problem unless we can quantify the neurons dying per minute. 1.9 million neurons dying per minute in stroke focused attention on speed of intervention. 
http://stroke.ahajournals.org/content/47/1/99.abstract?sid=9902c2fc-fc05-40fb-b6dc-2e313e0096c5

1. Hongyu An, DSc*;
2. Andria L. Ford, MD*;
3. Cihat Eldeniz, PhD;
4. Yasheng Chen, DSc;
5. Katie D. Vo, MD;
6. Hongtu Zhu, PhD;
7. William J. Powers, MD;
8. Weili Lin, PhD;
9. Jin-Moo Lee, MD, PhD

+ Author Affiliations

1. From the Mallinckrodt Institute of Radiology (H.A., C.E., K.D.V., J.-M.L.) and Department of Neurology (A.L.F., Y.C., J.-M.L.), Washington University, School of Medicine; and Department of Biostatistics (H.Z.), Department of Neurology (W.J.P., W.L.), and Department of Radiology (W.L.), University of North Carolina at Chapel Hill.

1. Correspondence to Jin-Moo Lee, MD, Washington University, School of Medicine, Department of Neurology, 600 South Euclid Ave, Campus Box 8111, Saint Louis, Missouri 63110, E-mail leejm@neuro.wustl.edu or Weili Lin, PhD, University of North Carolina, 106 Mason Farm Rd, Campus Box 7515, Chapel Hill, NC 27599, E-mail weili_lin@med.unc.edu

1. ↵* Drs An and Ford contributed equally.

Abstract

Background and Purpose—We aimed to examine perfusion changes between 3 and 6 and 6 and 24 hours after stroke onset and their impact on tissue outcome.

Methods—Acute ischemic stroke patients underwent perfusion magnetic resonance imaging at 3, 6, and 24 hours after stroke onset and follow-up fluid-attenuated inversion recovery at 1 month to assess tissue fate. Mean transit time prolongation maps (MTTp=MTT–[median MTT of contralateral hemisphere]) were obtained at 3 (MTTp_{3 h}), 6 (MTTp_{6 h}), and 24 hours (MTTp_{24 h}). Perfusion changes between 3 and 6 hours (ΔMTTp_{3_6}) and 6 and 24 hours (ΔMTTp_{6_24}) were calculated. A 2-step analysis was performed to evaluate the impact of ΔMTTp_{3_6} and ΔMTTp_{6_24} on tissue fate. First, a voxel-based multivariable logistic regression was performed for each individual patient with MTTp_{3 h}, ΔMTTp_{3_6}, and ΔMTT_{6_24} as independent variables and tissue fate as outcome. Second, Wilcoxon signed-rank tests on logistic regression coefficients were performed across patients to evaluate whether ΔMTTp_{3_6} and ΔMTT_{6_24} had significant impact on tissue fate for varying severities of baseline perfusion.

Results—Perfusion change was common during both time periods: 85% and 81% of patients had perfusion improvement during 3- to 6- and 6- and 24-hour time intervals, respectively. ΔMTT_{3_6} significantly influenced 1-month infarct probability across a wide range of baseline perfusion (MTTp 0–15 s). ΔMTT_{6_24} also impacted 1-month infarct probability, but its influence was restricted to tissue with milder baseline ischemia (MTTp 0–10 s).

Conclusions—Brain tissue with mild to moderate ischemia can be salvaged by reperfusion even after 6 hours. Such tissue could be targeted for intervention beyond current treatment windows.

Neuromechanical Factors That Limit Walking Speed in Individuals with Post-Stroke Hemiparesis

I'm sure your doctor/therapist can apply any new information in here to your updated stroke walking protocol.

http://gradworks.umi.com/36/26/3626475.html

Abstract:
Individuals, post-stroke, present with an array of changes to the neuromuscular system function such as muscle weakness and abnormal muscle activation patterns. Different combinations of these and other altered body functions result in limitations in functional mobility, such as reduced gait speed and high risk for falls. In this series of studies, I developed a deeper understanding of how neuromechanical factors may limit the fastest speed that an individual post-stroke can reach before they are unable to move any faster without losing balance. I conducted three studies. In the first study, my results showed that, after stroke, individuals have the capacity to walk at faster speeds than their overground self-selected maximum walking speed, while walking on a treadmill and when provided horizontal assistance using a robotic device. In the second study, I showed that non-impaired individuals modulated the amplitude and phasing of muscle activity according to the requirements brought about by the existence of horizontal assistive forces during walking at progressively faster speeds. Finally, in the third study I showed that individuals post-stroke also were able to modulate amplitude and phasing of muscle activity in both legs, according to the requirements brought about by the existence of horizontal assistive forces during walking at progressively faster speeds. However, the paretic leg was more responsive to horizontal assistive forces than the non-paretic leg. The understanding gained through these studies provide novel insights regarding the capabilities of individuals with post-stroke hemiparesis to adapt their existing impaired neuromuscular mechanisms into more challenging walking tasks. Each study leads to ideas for the development of potentially more effective rehabilitation protocols targeted at the modulation of amplitude and phasing of muscle activity in order to safely achieve faster walking speeds.

Adviser	David A. Brown
School	NORTHWESTERN UNIVERSITY
Source Type	Dissertation
Subjects	Neurosciences; Physical therapy; Biomechanics
Publication Number	3626475

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Need for Speed - Better Movement Quality During Faster Task Performance After Stroke

If I could do anything speedily I would try. If these participants could do 3 finger grasp they were pretty high-functioning already. Why not test someone who can't even open their hand? This is pretty much just testing undamaged neurons so look at your damage scans first.
http://nnr.sagepub.com/content/26/4/362.abstract?etoc

Abstract

Background. Although slow and insufficient muscle activation is a hallmark of hemiparesis poststroke, movement speed is rarely emphasized during upper-extremity rehabilitation. Moving faster may increase the intensity of task-specific training, but positive and/or negative effects on paretic-limb movement quality are unknown. Objective. To determine whether moving quickly instead of at a preferred speed either enhances or impairs paretic-limb task performance after stroke. Methods. A total of 16 people with poststroke hemiparesis and 11 healthy controls performed reach–grasp–lift movements at their preferred speed and as fast as possible, using palmar and 3-finger grip types. The authors measured durations of the reach and grasp phases, straightness of the reach path, thumb–index finger separation (aperture), efficiency of finger movement, and grip force. Results. Reach and grasp phase durations decreased in the fast condition in both groups, showing that participants were able to move more quickly when asked. When moving fast, the hemiparetic group had reach durations equal to those of healthy controls moving at their preferred speed. Movement quality also improved. Reach paths were straighter, and peak apertures were greater in both groups in the fast condition. The group with hemiparesis also showed improved efficiency of finger movement. Differences in peak grip force across speed conditions did not reach significance. Conclusions. People with hemiparesis who can perform reach–grasp–lift movements with a 3-finger grip can move faster than they choose to, and when they do, movement quality improves. Simple instructions to move faster could be a cost-free and effective means of increasing rehabilitation intensity after stroke.