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  #1  
Old 04-15-07, 05:22 AM
McHuman McHuman is offline
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Dopamine + ADD // Norepropine + ADD

Stimulants boost dopamine, but not Strattera.

How important do you think *dopamine* is for treating ADD? Is it really dopamine that ADDers lack? Or is it just the norepropine which matters?
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  #2  
Old 04-15-07, 09:47 AM
nzkiwi nzkiwi is offline
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That's a good question, I'm not really sure.

Perhaps dopamine effects attention and norepinephrine effects motivation(drive), just guessing. Perhaps for one person it's dopamine, another person norepinephrine, or even for some both neurotransmitters.

I've probably just opened a new can of worms.:foot:
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Old 04-15-07, 11:52 AM
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Well... at some synapses, both norepinephrine and dopamine are released. I believe the NET (norepinephrine transporter) that is responsible for reuptake also is responsible for taking in excessive dopamine (or maybe that's the other way around... DAT -> NE reuptake). But anyway, if you inhibit the reuptake on one, you may be doing it to the other.

So actually, Strattera does have an effect on dopamine.

Dopamine is responsible for motivation and attention, where norepinephrine is responsible for attention and memory (long-term). They are both believed to be important in ADD.

If the medication did not affect dopamine, it probably wouldn't have an impact on one's ability to tune out external distraction. In fact, it would probably be the opposite in that respect.
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Old 04-15-07, 03:10 PM
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ok, if dopamine is the problem, then why are we not showing parkinson's disease symptoms and why can't we just take levodopa (l-dopa) or natural l-dopa (mucuna pruriens) instead for medication?
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Old 04-15-07, 03:29 PM
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Quote:
Originally Posted by NICEEE
ok, if dopamine is the problem, then why are we not showing parkinson's disease symptoms and why can't we just take levodopa (l-dopa) or natural l-dopa (mucuna pruriens) instead for medication?
The amount of dopamine released in the synapse isn't regulated by the available amount. The medication affects (depending on the particular medication) how long the neurotransmitter stays in the synapse and some also cause the release of dopamine into the synapse (amphetamine). Parkinson's is a dopamine related problem, but is qualitatively different.

Also, having two disorders involving the same neurochemical does not imply that a problem with X neurotransmitter creates the same problem. Each neurotransmitter has different effects throughout the brain, and a problem with each neurotransmitter could be caused by different problems (lack of it (parkinsons), excessive reuptake (possibly ADHD), chemical insensitivity of post-synaptic neuron, etc.).
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Old 04-15-07, 05:36 PM
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this is interesting ...

http://en.wikipedia.org/wiki/Parkinson's_disease
Motor symptoms
The cardinal symptoms are:

-tremor: normally 4-7Hz tremor

http://en.wikipedia.org/wiki/Electroencephalography
Theta is the frequency range from 4 Hz to 8 Hz and is associated with drowsiness, childhood, adolescence and young adulthood.
This EEG frequency can sometimes be produced by hyperventilation.
Theta waves can be seen during hypnagogic states such as trances, hypnosis, deep day dreams, lucid dreaming and light sleep and the preconscious state just upon waking, and just before falling asleep.

~ ... ~

4 per second
8 per second
6 - is 360 per minute
[degrees]

4 per second ->- 1/4

1/4
and

360 degrees

~ ... ~
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  #7  
Old 04-15-07, 07:02 PM
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Is dopamine not the chemical that controls emotions?

I know that anti depressants increase the level of dopamine to give the patient an over whelming feeling of pleasure.

But I never knew stimulents had the same effect.....
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Old 04-16-07, 04:54 AM
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Quote:
How important do you think *dopamine* is for treating ADD? Is it really dopamine that ADDers lack? Or is it just the norepropine which matters?

The Dopamine Transporter and Attention-Deficit/Hyperactivity Disorder

Medications for ADHD interfere with dopamine transport by brain-region- and drug-specific mechanisms, indirectly activating dopamine- and possibly norepinephrine-receptor subtypes that are implicated in enhancing attention and experiential salience. The most commonly used DAT{solute carrier neurotransmitter transporter dopaimne}-selective ADHD medications raise extracellular dopamine levels in DAT-rich brain regions. In brain regions expressing both the DAT and the norepinephrine transporter (NET), the relative contributions of dopamine and norepinephrine to ADHD pathophysiology and therapeutic response are obfuscated by the capacity of the NET to clear dopamine as well as norepinephrine. Thus, ADHD medications targeting DAT or NET might disperse dopamine widely and consign dopamine storage and release to regulation by noradrenergic, as well as dopaminergic neurons.***End Quote

{part in these added by me for information perposes}


Hope this helps. . . . . .I know simply you asking the question helped me. . . .gotta a medical search engine bonus while looking your infornmation up. . .
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  #9  
Old 04-16-07, 05:12 AM
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Quote:
Originally Posted by SB_UK
Theta waves can be seen during hypnagogic states such as trances, hypnosis, deep day dreams, lucid dreaming and light sleep and the preconscious state just upon waking, and just before falling asleep.
Specificity of quantitative EEG analysis in adults with attention deficit hyperactivity disorder


The ADHD and control groups did not differ in beta activity, but relative theta was reduced and relative beta power was elevated in the non-ADHD group compared with both the ADHD and control groups. These results suggest that quantitative EEG may be used to differentiate ADHD adults from both normal adults and adults who display some of the symptoms of ADHD, but fail to meet the diagnostic criteria of ADHD.***End Quote

So by changing our neurotransmitters if effect they change our brian waves thus decreasing the ADD symptoms?

Makes sense strangly enough . . . .science making sense my world my crash all around me.

Well the forntal lobe thing looks like it might be a flop = like we are surprized.


Performance of children with ADHD on tests sensitive to frontal lobe dysfunction.

The performances of 20 children with attention deficit hyperactivity disorder (ADHD) were compared with those of 20 matched normal controls on a battery of neuropsychological tests. The ADHD children exhibited impaired function in reading comprehension, verbal learning and memory, and on the Information, Arithmetic, Digit Span, Block Design, and Coding subtests of the Wechsler Intelligence Scale for Children-Revised, but they performed nearly normally on measures of verbal and design fluency and on the Wisconsin Card Sorting Test. The hypothesis that disturbances in frontal lobe function related to impulse control may be responsible for the cognitive impairments observed in ADHD was not supported. Inability to control and direct attention appears to be more central to the pathophysiology of this disorder.
***End Quote

{bold and underlining mine}

Can any one say no shhhhht sherlock?
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  #10  
Old 04-16-07, 08:02 AM
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The problem is that different drugs work on different receptors, and that's why one drug may work for you and another won't, even though they both affect the same chemical. Someone who does great on one SSRI might have a horrible time on another because each affects a different serotonin receptor, which in turn will affect dopamine and norepinephrine levels later on because all three chemicals affect one another.

Now, it had occurred to Oliver Sacks to give certain patients l-dopa, and it worked for a while, and then the patients reverted back to their noncommunicative states. (A movie was made of this, I think it was called "Awakenings", but I don't know the title of Dr. Sacks' book.) The problem is that we don't know everything about the way the brain processes and/or blocks all of these chemicals. When I was on Wellbutrin and developed tics in my hands that resembled a Parkinson's-like tremor, it occurred to me as well that it should be looked into. Of course, I'd wager there are plenty of researchers out there who've figured that out already, and if it were that simple, there would already be a treatment.

I know that there are illegal recreational drugs out there that can permanently disable the receptors for serotonin, and I'd imagine that a lot of these neurological conditions involve receptor damage, so no matter how much of a medication you're given, nothing will change. Add in individual body chemistry and workings, and you have even more variables. Plus, the brain is only recently being effectively mapped, and its complexity is pretty daunting. Most of what neurobiologists are doing for people with depression, ADD, autism, schizophrenia, and so on is like a game of darts. You take your favorite dart, which has hit the target faithfully over and over and give it a throw - no matter how balanced and perfectly aimed, there's still a chance it's not going to hit the bullseye. Fortunately, though, the technology is still being explored, new treatments are always being tested, so with the ever-growing aresenal there's a chance that a medication that didn't work for someone will soon be joined by one that hits the mark. All we can do is keep trying and not give up.
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Old 08-10-08, 12:43 AM
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Re: Dopamine + ADD // Norepropine + ADD

Quote:
Originally Posted by meadd823 View Post
Well the forntal lobe thing looks like it might be a flop = like we are surprized.


Performance of children with ADHD on tests sensitive to frontal lobe dysfunction.

The performances of 20 children with attention deficit hyperactivity disorder (ADHD) were compared with those of 20 matched normal controls on a battery of neuropsychological tests. The ADHD children exhibited impaired function in reading comprehension, verbal learning and memory, and on the Information, Arithmetic, Digit Span, Block Design, and Coding subtests of the Wechsler Intelligence Scale for Children-Revised, but they performed nearly normally on measures of verbal and design fluency and on the Wisconsin Card Sorting Test. The hypothesis that disturbances in frontal lobe function related to impulse control may be responsible for the cognitive impairments observed in ADHD was not supported. Inability to control and direct attention appears to be more central to the pathophysiology of this disorder.
***End Quote

{bold and underlining mine}

Can any one say no shhhhht sherlock?
I'm not sure what the implications of this are? Are you trying to refute the studies that prove ADHDers have less activity in the frontal lobe regions?
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  #12  
Old 04-16-07, 09:27 AM
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Posted by Fraz 2006:
Quote:
I know that anti depressants increase the level of dopamine to give the patient an over whelming feeling of pleasure.
Really?!!?!! What kind of anti-depressants are you referring to here? I've tried plenty and have NEVER even come close to experiencing an "overwhelming feeling of pleasure." I certainly would like to, though.

Sue

Last edited by sloppitty-sue; 04-16-07 at 09:28 AM.. Reason: spelling
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Old 04-18-07, 01:01 AM
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Parkinson's is believed to be caused by decreased dopamine activity, specifically in the substantia nigra and the locus coeruleus. L-dopa increases dopamine in the brain, but not necessarily in the areas of the brain involved in adhd(frontal cortex, etc). It's not just the total level of dopamine in the brain, but the levels in specific areas that causes disease and disorders. The brain is a complex organ(three pound universe).
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Old 04-18-07, 08:12 AM
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"Three pound universe'!!!! I love it! A couple of days ago I heard someone say "Life doesn't have to be perfect to be wonderful" and I thought it would be my favorite phrase for quite a while, but this one deserves a place in the top ten, IMO.

The receptors are as important as the chemicals themselves, and as you said, if the chemicals don't go to the right parts of the brain, nothing's going to happen. While science is going a long way to learning how to fix things in the nervous system and brain, it performs so many functions in tiny specific areas that sometimes nothing can be done. Victims of strokes might be able to train the working parts of their brains to take over certain motor functions for the other side, but that's as far as we've gotten so far. In some patients who've had injury to a particular part of the brain, an adjacent part will try to kick in and help, but since it provides a different function it sometimes does more harm than good.

Essentially, if there's nothing wrong with the receptors a drug is formulated to target, the drug will do the patient no good. If the drug targets an area that is damaged, the drug will do the patient no good. Fortunately, we have a lot of scientists around the world who think that mapping the brain and figuring out how it does what it does is fascinating enough that even without the funding for the brain mapping project, they're going to keep plugging away and making progress.
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Old 04-18-07, 12:30 PM
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@Fraz_2006

anti depressants actually tend to for the most part increase serotonin, which has much more effect on emotion and no huge effect on pleasure. stimulants effect dopamine and norephenephrine for the most part which create feelings of pleasure while drowing out emotion (dopamine will replace serotonin when its flooded into the brain) - thats your difference
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