Posted by utopizen on May 31, 2006, at 5:53:14
In reply to Re: One year on Aricept- ADD augmenter, sleep boos » utopizen, posted by blueberry on May 26, 2006, at 15:33:19
> What exactly was it that prompted you to think a cholinergic mechanism was involved? It is great it has helped you so much. I am curious what led you in that direction. While it seems the entire world is looking at serotonin, dopamine, norepinephrine, and gaba, what was it that made you look at cholinergic mechanisms?
>Well... the thing to remember is, the "cholinergic mechanism" is at hand with basically everything.
It's also well-studied. And drugs that dry you up, like amphetamines, etc., are acting at the same parts of brain as Aricept, with certain variations.
Hence, why I needed to _REDUCE_ my use of Desoxyn. 10mg 2x/day became unpleasant, too much with the introduction of Aricept. I would hyperfocus, get agitation, all of the signs of overdose, at the normally prescribed dose all of a sudden.
So it potentiates existing effects a stimulant causes. This is because it's working on similiar mechanisms, increasing dopamine, etc.
So, not sure what you mean by that... um, Aricept is used for Altzhiemer's patients.
My mind tends to think in creative processes that seem as intuitive/instrinsic to me, and then when forced to explain how I arrived at what seemed "elementary, my Dear Watson" I notice the burden Sherlock Holmes has in having to explain how I came about something by connecting so many dots so rapidly and effortlessly.
I don't mean to suggest everyone who takes Aricept to add-on to their ADD regimen will become this creative, quick-witted, socially adept genius smooth talker with incredible charm (fortunately, pharmaceutical companies have failed in their efforts to emulate my essence).
Yet like Thomas DeQuincey makes clear in Confessions of an Opium Eater, a dull person who takes something like opium will have yet still dull dreams. He doesn't let people think someone unlike him who takes the same drug will be able to write a great literary work.
A drug that potentiates may only potentiate a potential.
Okay, that said, for my psychopharmacology presentation, I did have to go, "Um, utopizen, let's re-map how the heck you understood so much enough to actually be your own successful testbed." So, without having to reveal the fact I'm basically a walking case study and proud consumer of Aricept (lol) I did this the following way (in a very concise presentation that amazed my professor):
--First, what defines "cognitive enhancers"(Aricept, NMDA antagonists, amphetamines, nicotines, to be broad) is this:
they delay or reverse cognitive impairment.
(Antonyms really help to define something, especially when you want to broaden an entire class of drugs) ;)
--Second, what disorder do the existing use of the drugs show success, and how does this disorder parallel the target disorder to justify exploring similiar approaches to treatment?
Well, it's a geriatric drug, so, I found an interesting disorder that features Executive Dysfunction as a symptom.
Executive Dysfunction is also a symptom in about 1/3 of patients with AD/HD (while much of AD/HD may be reducable to varying levels of Executive Dysfunction, keep in mind it is separate and is a disorder of severity, not kind-- just like any mental/neurological disorder).
So, with that said, here's a handout. Quiz is Friday. Glad you asked for my response =)
➲ Understanding Concerns of Apathy:
A Correlate to Other Neuropsychological Deficits==> Primarily characterized by motivational loss–– loss of interest and drive to engage in goal-oriented behavior (Martin, 1990).
==> Features distinctively separate from mood disturbance (e.g., depression). Loss of interest and drive rooted in an emotional indifference, not dysphoria (Martin et al., 1994).➲ Three major subsystems implicated in apathy:
==> Dorsolateral Prefrontal Circuit— Executive Cognitive Dysfunction
==> Lateral Orbital Prefrontal Circuit— Disinhibition
==> Medial (anterior cingulated) Circuit— Motivation Disorders (e.g., apathy)
(Cummings, 1993)➲ Neurobiological Basis of Apathy Hypothesis:
==> Medial Frontal Lobe + Limbic Cholinergic Deficits
==> Dopaminergic pathways involved in frontal-subcortical activation
(Cummings and Black, 1998)➲ Pharmacological Treatments Presenting Statistically Significant Clinical Efficacy (P > .05):
==> Donezepil (Aricept ®),
==> Provigil (Modafinal ®),
==> Amphetamines (Dexedrine ®), Adderall ®),
==> Desoxyephederine / Methamphetamine (Desoxyn ®)
==> Methylphenidate➲ Nicotine as a Working Model for Executive Function Mediation
==> Schizophrenia and ADHD:
==> Nicotine stimulation enhances selective attention
==> Sensory detection, and inhibition processes in attention
poster:utopizen
thread:648509
URL: http://www.dr-bob.org/babble/20060530/msgs/650840.html