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Dexamphetamine vs. selegiline & cognative funcation

A

AlexxRed

Bluelighter
Joined
Apr 2, 2002
Messages
293
Location
melbourne, Australia
Hi all,

Another pysco stimulant question. I have heard many talk about the improved cognitive function especially memory while on a course of L-dep. Can anyone comment on the length of time before these improvements have been noticed?

I've read varying answers on from the selegiline thread so am asking again. Any comments?

What about in contrast to dexamphetamines used in low dose? Do their impair cognitive function, in terms of memory retention or have people noticed improvements?

I'd do more research myself, and plan to, but now I'm so busy at uni my head is spinning! So any feedback would be appreciated.

Cheers

Alex
 
The cognative function improvements of dextroamphetamine should be far greater than those of selegiline in most situations. Sure, technically amphetamine is a metabolite of selegiline, but the dosing is lower than one would be perscribed for dextroamphetamine.

And i've used amphetamines for a number of years and haven't experienced any sort of impairment of cognative function. Excessive abuse of methamphetamine could cause it for sure (well, any amphetamine could, meth is simply in a more abusable form), but as long as you moderate your use, it's highly unlikely you'll experience anything on that matter.

You can't mix the two, in case you don't already know, btw.
 
^^^^
yeah certainly know about not mixing the two...just wondering how you have found your memory on dex? or anyone else?

A few people have commented on almost photographic memory while on selegiline, something I certain don't get on dex. It is great for concentration & focus...I'm just wondering about its effects on memory recall.
 
Selegeline/deprenyl is far better in the sense that amphetamine can sometimes cause you to be distracted because of it's psychomotor stimulant effects, but beyond that I think it's down to the role of dopamine in directing attention & the reward from doing such (which is why hyperactivity - caused by not enough dopamine - is reversed by dopamine reuptake inhibitors like methylphenidate. When there's enough dopamine in the part of the brain - can't remember where at the moment! - concerned with attention & reward, the reward pathways mean that the person is content to continue studying - hence the paradoxical quieting effect of stimulant drugs)
 
^ nucleus acumbens?

Of the 3 I've tried for studying purposes: amphetamine / methylphenidate / selegiline.

Only methylphenidate has seemed useful for general studying.

I find selegiline gives a more manic feel, whereas methylphenidate gives me exceptional memory recall with little to no side-effects (other than I clean my house and exercise more!).

I've always found amphetamine to be too much fun to sit down and read 100 pages of text or so. To each their own.


(selegiline dosage was 5mg every 2 days, methylphenidate is just the plain 20mg dose whenever I want to put in some serious studying, amphetamine dose even at 10mg just got me too happy and excited to study).
 
^^^^^
The amphetamine does get me focused to study and I'm quite content to sit there and take notes, listen to lectures etc.

I'm only wondering about its overall effect on memory recall and if there are any associated negatives with retaining information?

Life is for living as you have had both:

I went for the dex because I had heard that many found dex to be much smoother, especially when coming off they commented a much more of a crash type feeling. Do you find this with methylphenidate? Do you get better sleep from it, or much the same?

When I got diagnosed (think with QEEG & EEG?) According to those results I have both noradrenaline and dopamine dysfunction which is why choose the Dex. I'm on a low does 10-15mg max

Fastandbulbous:

Do you have option on which is superior in general the methylphenidate or the Dex?. Understand it's personal choice just interested in your views.

I don't get many problems with distraction on Dex, I'm just wondering if the methylphenidate might be better for overall memory recall.

Also what about people who saying that there is much more of a slump, for want of a better word when methylphenidate wears off do you think there is anything beyond anecdotal experience/evidence in this??
 
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^ From my subjective viewpoint: I found methylphenidate to be the only drug that increased my memory recall. It seems to be "permanent" as in real learning, not just "cramming ability" that is lost 24-48 hours after the exam.

I've done 3 courses of selegiline... I guess my main "personal preference" problem is that the mild stimulation that it starts to give me a few days after taking it becomes annoying late at night and it takes me longer to fall asleep.

With methylphenidate it's in and out of my brain on a very predictable timeframe - as in I can sleep normally if I don't take any past 4pm or so.

I don't think I've read anything where there are "associated negatives" with methylphenidate/amphetamine - except of course in "recreational doses" or higher.

The only serious negative effect I got from selegiline was that it potentiated caffeine to the point where one cup of coffee would get me too anxious. I think it depends alot on your personal brain chemistry. I find drugs that affect dopamine more than norepinephrine more positive.
 
^^^

Well I'm in no position to start the selegiline anyway...too close to exams, but i'd be interested to see if the methylphenidate is of more benefit, especially in terms of memory recall. Do you just use the standard, or long release versions?

Thanks for the advice
 
I know it's not easy to get, but the best stimulant-like drug I've ever had w.r.t. learning/memory retention is pemoline. It's a mild CNS stimulant with a long half life, but isn't at all distracting in the way that I find amphetamine distracting.

The closest relative of pemoline's that you're likely to come across is 4-MAR & from what I've read about it, it does sound like almost the ideal drug for such purposes (sadly, I've never had it to be able to make a comparison)
 
AlexxRed said:
Life is for living as you have had both:
I went for the dex because I had heard that many found dex to be much smoother, especially when coming off they commented a much more of a crash type feeling. Do you find this with methylphenidate? Do you get better sleep from it, or much the same?

When I got diagnosed (think with QEEG & EEG?) According to those results I have both noradrenaline and dopamine dysfunction which is why choose the Dex. I'm on a low does 10-15mg max
Click to expand...

Well, I use methylphenidate as a *ahem* study aid, not really to treat a problem... but as I've read alot on Bluelight, there seems to be 2 "types" of people: "meth brains" and "coke brains". I've never really cared for amphetamine or meth - both just make me alert and anxious - not really fun or productive. Coke (in what seems like a previous lifetime now) was what gave me "superman" type euphoria... methylphenidate seems like the most functional drug I've tried.

Methylphenidate doesn't affect my emotions in any way negatively - and the weirdest thing about my "brain chemistry" is that there is *no* comedown from methylphenidate. I go from focused to sleepy - perfect for my lifestyle.

Amphetamine - inevitably - always ended with negative emotions and anxiety. Truly; stimulants affect different people differently :)

Also what about people who saying that there is much more of a slump, for want of a better word when methylphenidate wears off do you think there is anything beyond anecdotal experience/evidence in this??
Click to expand...

I find that if I do too much methylphenidate there is that dreaded "zombie" feeling, but funnily enough I've never had a problem with "wanting" to do methylphenidate to that point as there is no "rush" as there is with coke. Whereas if I was doing amphetamine I would want more to avoid the crash.

Regarding your diagnosis " (think with QEEG & EEG?) " I'm amazed they can tell anything about your dopamine/NE levels or dysfunction of them just by an EEG! I've read about the P300 "spike" that can predict a person's "impulse control"... but can they really tell what your DOP/NE levels are through those tests?!?!
 
^^^^

It was qEEGs & ERPs

They graphed THETA, BETA, THETA/BETA ratio, P300 amplitutue & latency

Topographic maps of my brain were used to measure Beta and Thea activity Looking at left and right hemispheres, midline, left and right frontal lobes.

A decrease in global Theta activity was seen to indicate dopaminergic dysfunction while Reduced Beta activity at 13 out of 17 sites was seen to indicate noradrenergic dysfunction.

(BTW this testing was done when I was 19, before any rec drug use.)

They used a oddball program to measure effortful sequential processing of information.

I think this Electrophysiological Assessment is data that supports or hinges on 'theory'. But hey at least they were pretty thorough rather than just handing me pills.

They might just show that everyone is different.

Having said that symptoms wise I do meet the requirement for an ADD/HD? diagnosis...and it is a pain in the ass.

To be honest long term I'm going to look at cognitive behaviour therapy, I think that surely I can program myself. At the moment, I'm just band-aiding it.

Anyway, I'm procrastinating...lol - I'd be happy to post some of the graphs & maps...be interested to see what people make of these theories
 
fastandbulbous said:
I know it's not easy to get, but the best stimulant-like drug I've ever had w.r.t. learning/memory retention is pemoline. It's a mild CNS stimulant with a long half life, but isn't at all distracting in the way that I find amphetamine distracting.

The closest relative of pemoline's that you're likely to come across is 4-MAR & from what I've read about it, it does sound like almost the ideal drug for such purposes (sadly, I've never had it to be able to make a comparison)
Click to expand...


pemoline is too hard on the liver, 4MA? 4-Methyl-Aminorex?

methylphenidate has too many negatives, i've read studies that purport dna damage and possibly being a carcinogen

good old amphetamine, is probably the safest hard mental drug in reasonable dosages, caffeine is thought to be safer, there are a few other pharmas like strattera or provigil and then of course there is the world of nootropics

as for selegiline, if i had to guess i'd say it was safer than amphetamine if you are matching it with other antioxidants (glutathione, catalase), but who knows? small doses do a lot for me (1.25mg eod) and i prefer to dose 6-8hr after 15mg dexedrine to help with any neurotoxicity

i generally get a lot of nothing done school-wise amped, i rarely take amps any more for educational purposes, that's what the prescription says but i hardly touch them and then only for recreation, though i quit smoking pot for the past 9 months of the fa/sp semesters, i smoked the other day and the amps went well with it, similar in some ways to pot with lsd, you can keep smoking and not be overwhelmed, though in this case i needed about 8 inputs and nothing was good enough, but that's really the drawback with amps, you need a hell of a good time to go with or you'll end up writing lengthy emails or blue light posts:)
 
AlexxRed said:
^^^^

It was qEEGs & ERPs

They graphed THETA, BETA, THETA/BETA ratio, P300 amplitutue & latency

Topographic maps of my brain were used to measure Beta and Thea activity Looking at left and right hemispheres, midline, left and right frontal lobes.

A decrease in global Theta activity was seen to indicate dopaminergic dysfunction while Reduced Beta activity at 13 out of 17 sites was seen to indicate noradrenergic dysfunction.

(BTW this testing was done when I was 19, before any rec drug use.)

They used a oddball program to measure effortful sequential processing of information.

I think this Electrophysiological Assessment is data that supports or hinges on 'theory'. But hey at least they were pretty thorough rather than just handing me pills.

They might just show that everyone is different.

Having said that symptoms wise I do meet the requirement for an ADD/HD? diagnosis...and it is a pain in the ass.

To be honest long term I'm going to look at cognitive behaviour therapy, I think that surely I can program myself. At the moment, I'm just band-aiding it.

Anyway, I'm procrastinating...lol - I'd be happy to post some of the graphs & maps...be interested to see what people make of these theories
Click to expand...

i suspect that a S.P.E.C.T. scan i one hundred times more informative of the brain than the test you took: Have a look at this site:

http://www.brainplace.com/bp/atlas/
 
^^^^

Very interesting. Totally agree that they would be a far better scan.

Just wondering about your experiences with Seleiline Dr. Beat? Did you find it effective for your ADD. Also just curious if you combined it with a low dose of sodium valproate?

Cheers

Alex
 
Selegeline/deprenyl is far better in the sense that amphetamine can sometimes cause you to be distracted because of it's psychomotor stimulant effects, but beyond that I think it's down to the role of dopamine in directing attention & the reward from doing such (which is why hyperactivity - caused by not enough dopamine - is reversed by dopamine reuptake inhibitors like methylphenidate. When there's enough dopamine in the part of the brain - can't remember where at the moment! - concerned with attention & reward, the reward pathways mean that the person is content to continue studying - hence the paradoxical quieting effect of stimulant drugs)
Click to expand...


That is basicly the existing theroy of ADHD Fab but it has alot of holes in it. For one, Stimulants in ADHD are not acting on the reward centres of the brain as the as the dose is far too low and if it was and you were feeling all happy I dunno about you but the last thing I would want to do is study. I would want to jump up and down and put on some music that goes Doof Doof Doof. Also, there is nothing Paradoxical about the effects on stimulants with Adhd, rather than stimulate the reward centres of the brain it appears rather than they stimuate the inhibitory centres of the brain

From http://www.psychiatrictimes.com/p960738.html

Research in developmental psychology and neuropsychology have shown behavioral inhibition to be critical to the effective performance of several cognitive abilities considered executive functions because they are related to self-regulation. Not surprisingly, then, researchers in ADHD have begun to view ADHD as a disorder of self-regulation (Douglas) or executive function (Denckla), although both terms are vague when employed in this regard.

Nevertheless, the trend to a broader conceptualization of ADHD seems necessary given the variety of studies that either demonstrate or at least hint that ADHD children have deficits in working memory and sense of time; the cross-temporal organization of behavior; the internalization of speech and rule-governed behavior; the self-regulation of emotion and motivation; and the execution of complex, novel behavioral sequences (Barkley, in press). All of these are deemed executive functions and all seem to permit control of behavior by internally represented information.

Far more research is needed on these cognitive functions to cement their association with ADHD. However, the extant research offers the exciting possibility that ADHD is actually a developmental disorder of self-regulation, arising from a deficit in behavioral inhibition that in turn causes a deficiency in behavior regulation by internally represented information or events. If so, the hyperactivity and "inattention" (poor persistence/distractibility) seen in ADHD children and adults may simply be the most obvious (and most superficial) signs of a deeper, more pervasive, more socially significant disorder than has heretofore been imagined.
Click to expand...


Executive functioning in adult attention-deficit hyperactivity disorder.

Rapport LJ, Van Voorhis A, Tzelepis A, Friedman SR.

Department of Psychology, Wayne State University, Detroit, MI 48202, USA. [email protected]

The present study examined the executive abilities of 35 adults diagnosed with Attention-Deficit Hyperactivily Disorder (ADHD) and 32 adults without the disorder (n = 67) who were equivalent in age, gender, years of education, and Full Scale IQ. The ADHD group performed significantly worse on Stroop Color-Word (eta(2) =.18) and Interference (eta( 2) =.08), as well as time to complete Trails B (eta(2) =.08) than the controls (all ps <. 05). Analysis of Design Fluency indicated that the ADHD group committed more perseverative (eta(2) =.06) and non-perseverative (eta(2) =.12) errors than did controls; however, novel output was equivalent for the groups. No group differences were observed on tests measuring cognitive initiation, abstract thinking, or working memory (all ps >.30; eta(2) =.00-.01). The distributions of WCST variables showed severe skew associated with high-functioning performance on the test among both groups. The pattern of results suggests the presence of specific deficits in response inhibition, with intact abilities in other cognitive domains, such as primary verbal and visuospatial skills. These findings are consistent with the literature on neuropsychological deficits among children with ADHD. That persons with ADHD present a primary deficit of behavioral inhibition supports Barkley's (1997) theory of ADHD, as opposed to theories by Denckla (1996) and Roberts and Pennington (1996) that emphasize intention and working memory
Click to expand...


http://www.ncbi.nlm.nih.gov/entrez/...uids=11935449&query_hl=24&itool=pubmed_DocSum



The relation between disinhibition and emotion regulation in boys with attention deficit hyperactivity disorder.

Walcott CM, Landau S.

Department of Psychology, Illinois State University, USA. [email protected]

This study examined group differences of 49 boys ages 6 to 11 years with and without attention deficit hyperactivity disorder (ADHD) in emotion regulation during frustrating peer competition. Half of all boys in each group were explicitly instructed to hide their feelings if they became upset during the competition. Behavioral inhibition, both before and after the competitive task, was examined using the Stop Signal Task (SST), and emotion regulation was assessed via structured observation data. Effect sizes indicated that impulsive ADHD boys displayed greater disinhibition and were less effective at emotion regulation than comparison boys. In addition, boys with ADHD were unsuccessful in masking their emotions even when instructed to do so. In contrast, comparison boys were more successful at emotion regulation when given instruction to self-regulate, and these regulatory attempts predicted later inhibitory control. Findings are discussed in the context of current ADHD-related theories of inhibitory deficit, and suggestions for future research are provided.
Click to expand...

http://www.ncbi.nlm.nih.gov/entrez/...uids=15498744&query_hl=24&itool=pubmed_docsum

Effects of acute nicotine administration on behavioral inhibition in adolescents with attention-deficit/hyperactivity disorder.

Potter AS, Newhouse PA.

Clinical Neuroscience Research Unit, Department of Psychiatry, College of Medicine, University of Vermont, 1 South Prospect Street, Burlington, VT 05401, USA.

RATIONALE: Adolescents with attention-deficit/hyperactivity disorder (ADHD) become cigarette smokers at twice the rate of non-ADHD adolescents, and this finding continues into adulthood. Abnormal cognitive/behavioral inhibition is one core cognitive symptom of ADHD, leading to impulsive behavior in people with this disorder. Nicotine, contained in tobacco smoke, is known to improve attention, vigilance, and short-term memory. However, little is known about how nicotine might effect cognitive/behavioral inhibition. OBJECTIVE: This study tested the hypothesis that acute nicotine administration would improve cognitive/behavioral inhibition in non-smoking adolescents with ADHD. METHODS: This single-dose, acute, repeated-measures, double blind study in adolescents (13-17 years) with DSM-IV confirmed ADHD assessed the effects of transdermal nicotine, oral methylphenidate, and placebo on inhibition in non-smoking adolescents with ADHD. Dependent measures included tests of cognitive/behavioral inhibition (the stop signal task), cognitive interference control (the Stroop task), and a measure of verbal learning and recognition (the hi-low imagery task). RESULTS: Results from five subjects indicated that stop signal reaction time (SSRT), an estimate of the speed of inhibiting a response, was significantly (P<0.01) improved following both nicotine and methylphenidate treatment as compared to placebo treatment. Neither "go" reaction time nor accuracy showed any effect of drug. In the Stroop task, another task of cognitive inhibition, nicotine but not methylphenidate significantly (P<0.05) decreased the Stroop effect compared to placebo. CONCLUSIONS: These results indicate that nicotine administration has measurable positive effects on cognitive/behavioral inhibition in adolescents with ADHD. The size of the effect is at least comparable to methylphenidate. Positive effects of nicotine on inhibitional performance may contribute to higher rates of cigarette use in adolescents with ADHD.
Click to expand...


ADHD is not an attentional Problem, it is one of inhibition, it is directly related to executive funtion. One test that springs to mind was where they had to groups of kids one with ADHD, one without and put them in front of a tv screen. On the screen sequence of numbers would flash up, their role was to push a button every time a number was repeated sequentually.
Basicly a very boring task and the non ADHD kids far out preformed the ADHD kids.
But when they added extra numbers flashing in the corners of the screens to make it more challenging (ie a stimulating) the difference between the groups was removed, the adhd kids were as good as the control kids.

Why?

Because the extra stimulation of the challenge released hormones in the brain that activated the inhibitory centres (ie executive control) of the brain that are understimulated usually inabling them to concentrate.

In another test they had a class with some adhd, some control students, they set them to work on a task and periodically they would distract them, with a noise, some kind of visualy stimulis etc. What they found was that the ADHD kids took 3 times as long to refocus an the task as controls. They also redifined what concentration really is that being constantly bringing yourself back on task from minner distractions, an itch, adjust yourself in your seat, stretching you shoulders etc etc etc. Basicly it says there is no such thing as concentration persae, only inhibition and the degree thereof.

Damn I wish I could find references for these
Check out this book by Dr. Russell Barkley "taking Charge of adhd) this is where alot of what I say here comes from. This is a brief run down of his argument

http://www.pubmedcentral.gov/pagerender.fcgi?artid=1188963&pageindex=1#page

That is why there is nothing paradoxical about the effect of stimulants on adhd peoples brains. They activate the executive control centres of the brain allowing them to filter out all the bullshit around them. It is why adhd people never finish tasks, education, relationships once the excitement is gone because they just can not think, their frontal lobes are switched off. This theroy also explains how ADHD people can Hyperfocus http://en.wikipedia.org/wiki/Hyperfocus something that the existing DSM criteria doesn't even recognise

ADHD people can concentrate just fine, when it interests them :) It should be renamed as "Behavioral inhibition deficet Disorder" cos that is what it really is.
 
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^^^^

Well I'd love some of that 'hyper focus' for my exams that are comming up!

My real question is if stimulants such as dexamphetamine might infact impair cognative function; specifically retention of information. I've found some things on pubmed, such as this:

We examined the effects of motor, verbal, memory, and spatial attention task during fMRI in 18 healthy volunteers. Functional MRI measurements were obtained at baseline and again 75 min after an oral dose of 25 mg dextroamphetamine. RESULTS: Dextroamphetamine caused a decrease in the number of activated pixels and the magnitude of the BOLD response during the three cognitive tasks tested but not during the motor task. These changes were region and task specific. CONCLUSIONS: This is the first study to examine the effect of dextroamphetamine on the number of activated pixels and the BOLD response during the performance of a range of cognitive and motor tasks. Our results suggest that dextroamphetamine causes measurable decreases in brain activity in a variety of regions during cognitive tasks. These changes might be linked to behavioral changes observed after dextroamphetamine administration and could possibly be mediated by alterations in dopaminergic activation.

http://www.ncbi.nlm.nih.gov/entrez/...tool=iconabstr&query_hl=2&itool=pubmed_docsum

Any comments?
 
I have noticed imparment from both, yet my memory has always been shit so whos to say........now what was I saying??...8(
 
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