All of us suffering with mental disorders must become educated about our disorders to be effectively helped by medical professionals.
The primary cause for psychiatric failure is the medical professions failure to make sure we become educated about our disorders. The medical community assuming their responsibility for our education will be the singular factor that will most dramatically improve psychiatric success rates.
Please read my reasons for emphasizing the importance of patient education and the strong assertions I made above.
The members of this board are my finest teachers.
The best teachers are those that can move us into new lines of thought, gestalt producing, dot connectors that assemble many fragmented chunks into one coherent object we call understanding.
That's you, all of you.
For example, in essence Thunor replied to "Alice" that [stimulants can't possibly be sleep inducing, insomnia has to be the unseen active ingredient.] I thought, Thu has to right. I can use Adderall to "induce sleep" when ADHD rebound prevents me from succumbing to normal exhaustion. But there is something missing. What the hecks is it?
Once the call is made to my low level curiosity object interface, I'll pursue the scent like a coon dog especially when reinforced by a genuine need for me to know.
The connective stimulus came from JaneWhite. She explained to me that my description of steroid effect was a description of excessive steroids.
Oh yeah, 5 million candle watt gestalt time, boy and girls.
It's how I found the level of education important for us to achieve as patients to get the best therapies possible from our medical professionals.
Our broad based layperson definitions of terms such as fatigue, sleepiness and tiredness make them synonyms for the same normal reaction. We use the same words to describe symptoms too. Most of us, including me until a few days ago, vaguely thought that "somnolence" was a $1.50 high sounding synonym. No one has ever heard me say, "I'm so somnolent, I got to quit. Hit the hay time." Never. The word isn't in my working vocabulary. I'll continue to use a description instead.
All medical professionals assign a far more specific meaning to the words mentioned above. Good doctors will try to disambiguate our broad based meaning into specific meanings they need to know to prescribe the best therapies. Regardless of doctor professionalism, and doctor type, specialists or GPs, they end up making an educated guess on specific meaning. Then, when able, they'll order tests to confirm or narrow down their ballpark suspicions to a specific diagnosis.
Many objective tests can be used to determine organ and system malfunction. Test for all likely physical possibilities for attention deficit symptoms. Then go to psychological testing (albeit most subjective) to narrow the search to mental disorder categories.
None of the above eliminates the need for patient education especially in the case of chronic mental illness. I throw ADHD into the chronic bucket since I've had it my entire life. Education is so essential for us because there are NO objective tests that can narrow down the diagnosis well enough to eliminate the time consuming, frustrating and detrimental trial and error process to finding the best therapies for our unique case.
I read recently a report by a respected psychiatrist researcher directed to other professionals in the psychiatric community (not us) "to assume their responsibility for patient education. Help your patients to become educated about their illness, able to differentiate symptoms and assign to them the correct medical word, to help them help you diagnose." Powerful advice, I'll bet goes mostly unnoticed.
There is little need for us to learn new words. The need is for us to learn the specific medical definitions to the words we already know.
As a community we spend more time barking up dead trees than anything else. The medical community has forced us into "do-it-yourself" education by leaving us without direction.
A resource in addition to our community is needed.
I'd like to see a series of study courses written and directed by teams of psychologists, neurologists, psychiatrists AND ADHD patients like us, specifically for us.
If you know of existing resources, please post them. I've seen some excellent ADHD 101 resources. Now that I have the terminology prerequisites, I can read research study reports with understanding.
The courses between 101 and the ADHD ADHD (Adhd Doctorate for Humans with the Disorder) [dang good acronym, eh] are missing.
A chapter or a section of the course toward your ADHD degree could be devoted to common words with medical definitions.
Fatigue - is a normal response to hard physical effort. It is felt in our muscles and bodies in general. It can include mental fatigue. Fatigue becomes a symptom when it becomes disassociated from its normal stimulus or out-of-proportion to its normal stimulus. Numerous sxamples are given. Sleepiness may or may not accompany fatigue or lead to sleep.
Mental Fatigue (Somnolence is associated with mental fatique) is a normal response to hard mental effort. It can follow excessive stress or from an extended period of stress. Somnolence becomes a symptom when it becomes disassociated from its normal stimulus or out-of-proportion to its normal stimulus. Sleepiness may or may not accompany somnolence or lead to sleep.
Sleepiness - Is the normal time-for-sleep call from our bodies. Sleepiness becomes a symptom when it becomes disassociated from its normal stimulus or out-of-proportion to its normal stimulus. Sleepiness leads to sleep.
Many more common words are used to describe reactions and symptoms associated with sleep and its disorders.
Now, I'll play shrink and patient.
Dr. Bob, "Bob what side effects do you experience from Adderall?"
Bob, "Somnolence, somnolence dude, I'm talking big time somnolence, get it?)
Dr. Bob, "I get it. So you aren't really knocked out belly up on the floor unconscious as you claimed to your former doctors."
Bob, "No doc, I ain't. Former doctors are still bozos, though, unable to read through my layman's description. I exaggerated in hopes of getting though. Their fault, not mine."
Other sections of the course leading to our ADHD degree would include neuroscience biology presented in a way we can easily grasp. If the course uses illustrations and examples everyone finds familiar, everyone will understand.
I can give a billion examples, here is one.
I was reading about how neurons (brain cells) shift polarity. Huh, I thought, what the hecks u talking about?
I thought about an unconnected battery. The potential on one end is positive and the other end negative. No juice flows. I could grasp fairly easily that once the potential on the presynaptic side got high enough, it causes a "spark" the same way as lightning. Our figurative "spark" pops open preloaded containers full of norepinephrine or another neuro. The discharge closes the circuit within the sending neuron effectively resetting it. Concurrently the neuro chemicals released are picked up by their receptors on the other side of the synapse.
The above is a chuck of info that had no meaning to me until understanding the role of neuro chemicals and their receptors and how psychotropic medications can be of immense benefit.
Each neurotransmitter has receptors of the same type. The neuro chemical will not bind to any other type receptor or will its receptors bind with any other neuro chemical. Overwhelming circumstantial evidence and reams of objective scientific evidence are strongly suggesting that a fault in the neurotransmission synaptic communication system in and between neurons is what causes us our problems.
In some cases, insufficient neuro chemical in the synapse is responsible. "Oh, finally, we have the freaking problem defined. About time. Good grief, if took em any longer I'd be dead. We can now "simply" solved the problem."
Let's use norepinephrine as an example because of its role in attention.
A synaptic norepi shortage? No problem. Researchers can isolate and synthesize norepi. I'll buy me a six pack of norepi and drink it.
Doesn't work. Waz the matter? The dang brain/blood barrier.
I must say, that the greatest contribution that psychiatry has made toward managing mental disorders of all types, is in the development and the continued refinement of psychotropic medications.
These meds are able to get past the brain/blood barrier. Medications that are designed to stimulant more norepinephrine look so similar to real norepinephrine that they bind with norepi receptors and trigger the response the receptors should have given all along.
Problem solved. Well, not quite, but we are on our way to a solution that can be satisfying efficacious for each of us.
My "conceptual" understanding of basic neuro system functioning is accurate enough for me to appreciate a few realities with enormous consequence.
I'm confident that my conclusions I express next are as accurate as you can get.
The solution to our woes is found in therapies that impact synaptic neurotransmission.
For some of us, natural supplements, good diet and exercise can turn the trick. All of us should implement good diet and exercise programs and avoid substances such as alcohol that are particularly damaging to us.
Another area to look at is environments we find overly stressful and avoid them if possible.
Still coming up short on managing ADHD symptom control?
You are a fool if you fail to get your ADHD degree.
You are a fool if you irrationally reject psychiatry and the available medications that can help you. These meds, when properly administered, balance brain chemistry restoring them over time to their natural state.
Want to talk about "unnatural?" Rejecting psychiatric care is the most unnatural thing you can do to yourself. Your brain will stay as unnaturally screwed up as the brain of a speed freak.
Jane, consider this my fecis for my ADHD degree. Thu, you make me think entirely to hard. I'm exhausted. Stop it. NOW.
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Bob, are you aware of NeuroPsychiatry? You might do some research into it.
I have ADD but I also have Multiple Sclerosis (MS). ADD meds are used for what is known as MS fatigue and have been known to help many. Stimulants, in general put me to sleep. I am also very med sensitive.
I don't know which thread steroids was discussed but....
Steroids can cause someone to have more energy and insomnia, however, some who use steroids find they make them sleepy.
Dx RRMS 1985
5/9/13/ Secondary Progressive WITHOUT Progression
Bob, are you aware of NeuroPsychiatry? You might do some research into it.
I've done a little research and should do more. A neuropsychiatrist is trained in neurology and psychiatry and has demonstrated competency in both, correct?
I'd like to see a resource developed by neurologists, psychiatrists and psychologists that includes patient perspective to help us better understand what ails us.
Not long ago I felt that there was little agreement within these professions much less between them. Reading research study reports written for medical professionals has totally eliminated that misconception in my mind.
The misconception comes from uncredentialed sources and sour grapped anedotes often after a buck found all over the Internet that present their opinions as evidenced based fact. Got to go to the horses mouth to find the truth.
Us humans can't be defined as "brains" or "adrenal glands" or "nerve connections interfacing with muscle cells." We are a unified, highly complex, system. I swear, it won't surprise if a break in a toe subsystem can cause psychosis. I'm talking delusional hallucinating crazy off the wall nuts cuz of a stubbed toe. Maybe not.
A few months back I did a "speedread" on guanfacine and was impressed with it ADHD effacious properties especially for ADHD rebound. So I run off to my shrink, ask for guanfacine for my insomnia that I think is the result of ADHD rebound. He sends to GP and I ended up with a prescription for clonidine. Clonidine did not help me.
I suspected the reason was my shrink and GP consulted and decided clonidine would be better for me. I realized that I did not make myself clear. I went in unprepared to a sales meeting with shrink to sell the idea of guanfacine for me. I know my shrink. I know if I presented my case convincingly, he would have agreed.
I'm so glad things went south on first "Intuniv" try. It forced me to follow your good example and actually research and study the properties of clonidine and guanfacine. Both are alpha-2 norepi agonists. Guanfacine is of subtype alpha-2A. The difference in the properties between clonidine and gaunfacine has to be found in the subtype alpha-2A.
So off I went into a hyperfocused quest to get the "why." About 30 hours of study time later, I understood ONE thing about neurons. Neurons are typed to neurotransmitters.
One type of neuron is of type norepinephrine. Norepi neurons have all the norepi receptors. The different norepi subtype receptors act as logic gates. These gates control the path of norepi and its quantity from its one source to its gadzillion possible destinations.
Sooooooooo, the dif between clonidine and guanfacine is the first acts on all alpha-2 receptors, the second on just alpha-2A. The results are: Clonidine ends up at more destinations so clonidine has a much broader set of properties. One of clonidine's properties is sedation. Sedation is NOT a clonidine side effect. Clonidine can be used to sedate the side effects of stimulants.
Guanfacine, on the other hand, is much more selective on alpha-2A receptors. The norepi logic gates set the path to fewer destinations. It so happens that one of the few is the prefrontal cortex area.
Sidebar: Once the path to destination is established, norepinephrine changes role from neurotransmitter to neural hormone. A region of the brain is activated. The neuro guys can see the region "light up" using SPECT scans or fMRI's. Pretty convincing evidence that theory of action is very close to actual action.
Suppression of ADHD rebound is a NOT property of guanfacine. Guanfacine's properties include improved working memory - NOT ADHD rebound. ADHD rebound is working memory gone wild. Clonidine, on the other hand, disrupts working memory. Clonidine made my ADHD rebound worse.
Does the biology translate to guanfacine actually helping me? I wrote an email to my GP briefly explaining in lucid detail why I want guanfacine, not clonidine. Granted, we had my clonidine history now, nevertheless, two days later, her office called to tell my guanfacine prescription was called in to Walmart YESTERDAY. I think my presentation had something to do with it.
Guanfacine is working BETTER than expected. I experience no, no, no, ADHD rebound. I mean finally NO ADHD rebound. About a week later, I visited my shrink, gave him a copy of my memo to GP, and shrink said "why didn't you tell me? Yes, of course, guanfacine is for you."
For the first time in a situation like that, I kept my mouth shut. I knew I did tell him that but not in a very clear or in a convincing manner.
Actual experience proved to me the value of getting your ADHD (Adhd Doctorate for adult Humans with the Disorder) degree. I do so love that acronym. One of my best.
Now that I got my ADHD degree, I must switch back to my job that makes money, money, money. Sing along with me - "I owe, I owe, it's off to work I go."
PS I must add one more facinating thing. We have epinephrine and norepinephrine. Transistors are grouped in CPU's to form logic gates And, Or, NotAnd (Nand), NOTOr (Nor). Hmn, Epi and NotEpi (norepi). Hmn, what explains the similarity in designation. Simple. Us humans learned math first, than applied it to computer science, now we apply the same math to neuro science. My background came in handy in wrapping my warped brain around neuro basics.
There is a difference in brain chemistry between men and women. The testosterone to estrogen ratio is 10:1 in young adult men:women. The hormone testosterone is connected to the neurotransmitter dopamine, estrogen to norepinephrine. Neurotransmitters maintain ratios (balances) between themselves.
A rarely discussed side effect of norepi and/or dopamine meds is the suppression of serotonin. The manifestation is usually different between men and women. Women become anxious and depressed because the serotonin to norepi balance becomes more out of whack. The greater dopamine to serotonin inbalance more often causes men to become anxious and angry. "More often" does not equal "always."
For similar reasons, girls more often display ADD and boys more often display ADHD.
Gender is yet another of the many, many variables indicating the medications must likely to help.
Why Norepinephrine Reuptake Inhibitor Medications Have Some Effect on Dopamine
If you strip off the outer insulator of your Cat5 network cable (used on home networks if not using wireless), you'll see several pairs, two wires each, twisted together. Twisting wires together insulates them from "cross talk" (unwanted signals called noise) from other wires wrapped in the same outer insulation of the cable.
According to a theoretical neural model proposed by neuroscientists, the brain runs parallel dopamine and norepinephrine neuron "wires" to destinations that require multiple neurotransmitters to activate and maintain attention and focus functions in demand. The two paths, one for dopamine and the other for norepinephrine, have limited insulation between them allowing for a degree of "cross talk." Norepinephrine reuptake inhibitor medications cause some dopamine reuptake inhibition as a result.
Attention and focus functions are equally dependent on dopamine and norepinephrine among a slew of other neurotransmitters that evidently play lessor roles.
I haven't researched this particular question, but another possibility, working from my limited understanding is that:
a) Dopamine and norepinephrine are chemically very similar, dopamine being a precursor of norepi, thus perhaps they share receptors in some cases? If this is the case, what blocks receptors for one might block receptors for the other?
b) As dopamine is the direct precursor of norepi, increasing the ready supply of norepi would then decrease the demand, which would lead to less dopamine being converted to norepi, thus increasing the available supply of dopamine?
No idea if these are plausible, just ideas that came to mind when reading your post.
On A) The best the neuro guys can figure it is dopamine and norepinephrine do not share receptors.
On B) I'll bet you are describing the "cross talk" mechanism assuming the "theoretical" working model is true.
Another factor to consider is that we are entering an area where even top level research leaders are uncertain as to the actual mechanisms involved.
Your stuff, as always, is very helpful. Please keep it coming.
Bottom line fact: SNRI's have some positive effects that increase available synaptic dopamine.
My theory on the meds: It appears to me that the NRI, Wellbutrin, has the most impact on dopamine, Strattera seems to have the least. The SNRI's appear to have similar positive effects. None of them increase available dopamine sufficiently to be helpful controllers of ADHD symptoms in most cases. Their usefulness is mostly as stimulant adjuncts.
You done did it again. Made me think, this case, think deeper.
I have a better understanding of neuron internals. Neurons may have over 1000 dendritic branches and each dendrite branch may receive thousands of synapses. Thus each neuron receives thousands of input signals through neurotransmitters bridging each synaptic clef. If the neurotransmitter binds with the receptor type, it results in a small electrical charge in the membrane of our postsynaptic neuron. Key point: The neuron will not fire an action potential until the sum of all of its synaptic electrical charges (potentials) at any one moment equals or exceeds its threshold.
Our neuron has one output cable, its axon. Its singular axon has many terminals. All axon terminal branches output the same neurotransmitter signal. The principle of "one neuron, one neurotransmitter" does have exceptions in motor and auditory neurons but remains true in our discussion limited to norepinephrine and dopamine transmission. Norepi and dopamine are not processed by the same type neuron.
But they most certainly influence each other.
Norepinephrine has a 3 stage reuptake system.
Uptake1: When the receptors on the postsynaptic side are "satisfied", molecular forces moves the transportors carrying the NA back into the presynaptic neuron.
Uptake2: Norepinephrine is sucked into nearby non-neuronal cells. Dopamine assists Uptake2.
Uptake3 or Vesicular uptake. Norepi transported back via Uptake1 into the presynaptic neuron is transported by VMAT into its containers - vesicles - completing the recycling process. Dopamine aids norepinephrine vesicular uptake.
Because dopamine does not share receptors with norepi does not mean dopamine has no influence on available synaptic norepi. Dopamine is very much involved in the reuptake of norepinephrine. Uptake2 sucks up spent norepi that can not be recyled. Dopamine is part of Uptake2 degradation that is partly responsible for signal termination. On the other hand, dopamine is a component of the vesicular uptake system. If vesicular uptake is inefficient, the vesicles have insufficient norepi available to release into the synapse. More norepi is transported into the synapse because of dopamine's role in vesicular uptake.
Dopamine increases synaptically available norepi using the same mechanism as guanfacine. Guanfacine, as a alpha-2 norepi agonist, should help, not inhibit reuptake. Guanfacine, like dopamine, helps the VMAT transporter. VMAT = Vesicular MonoAmine Transporter. Receptors are the primary norepi neuron to neuron signal flow controllers but only one of many signal senders controlling inter-neural functioning.
It reminds me of what a former U.S. President said. "I did not have sex with that woman." True, if oral sex is not sex. Dopamine and norepinephrine are in bed banging each other sans receptor intercourse. Norepinephrine facillates dopamine production too.
I was able to clear up one of my misconceptions. My understanding that neurons are typed to neurotransmitters appears to be accurate. However, my understanding that, for example, all norepi neurons have the entire set of norepi receptors, is incorrect. I assumed that on each call, the subset of activated norepi receptors acted as path switching logic gates. False. Absolutely false. On the contrary. It appears that the paths from norepi source to norepi destinations are hardwired. Neurons with receptors of type norepi alpha-2A agonists appear to be the path or one of the paths to the area in and around the prefrontal cortex. The neural transmission system is designed to transport norepi to the areas with high demand and conversely not transport norepi to areas with concurrent low demand.
People without ADHD can build greater pathway connectivity by mental exertion. Continually learning and improving their knowledge base and skills loads attention and focus functions. The neural pathways respond by forming more synaptic connections. To quote board member, "Free in Freepor;" "Neurons that fire together, wire together." The increase in synaptic connections is a type of memory. Mental exertion helps improve attention and focus skills. But not when ADHD disables the biological neurotransmission strengthening mechanism. We end up with a grossly underdeveloped neuro transmission system in spite of our best efforts.
I have good reasons to believe that ADHD medications can do more than control. In many cases the medications can fix the disorder if the patient works their brains hard while taking the meds. In that case, the temporary control that the meds offer can become permanent given enough time.
There are circumstances and co-existing disorders and diseases that may make a permanent fix impossible.
I like to see two additional sub topics added to this thread. 1) Why CBT is an important part of ADHD symptom control. 2) The symptoms of medication caused imbalances that can be used to identify the causative med and help find an effective solution.
For example, it seems that anxiety indicates an excessive norepi to serotonin ratio. Alternatively it may indicate an excessive norepi to dopamine. Or perhaps excessive norepi to serotonin and dopamine balance is out of whack.
Many doctors feel the best and only solution is to discontinue the medications. That approach itself has one very serious side-effect. It leaves us without control over our ADHD symptoms. I find it totally unacceptable. We can use a little education on medication solutions that can offset ADHD medication persistant side effects without killing ADHD control.
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Your understanding of neural biology now clearly outstrips my own. I will definitely test your theory of the 'permanent fix,' however, and have also determined to work harder at my homework! *Makes note to order 'Brain Fitness Program'*
I am as dumb as dumb gets. I'll prove it to you. I am familiar with the math and some of the constructs applied to neuroscience. More often than not, my background helps me grasp basic neural mechanics faster than otherwise. How accurately? Probably not accurate enough to pass the most basic neuro science test. Almost accurate enough for our purposes? I'm not there yet but closing in on the target.
My knowledge base doesn't stop me from drawing really stupid conclusions based on really stupid logic. One of my better examples of just how low my dumbness can go is concluding that NORepinephrine prefix NOR is derived from the NotOr (NOR) logic gate and its C++ logic operator expression. The logical results returned from "if NOT(epinephrine==epinephrine OR norepinephrine == epinephrine)" would be there is no chemical that is epinephrine including epinephrine itself. In utter words, there ain't no such thing called epinephrine.
The NOR prefix is derived from NORmal. Chemically, the word "normal" is used to indicate the absence of a radical group, usually methyl. Epinephrine has the radical methyl compound. I guess we can use half of my bassackwards logic afterall. How bout "NOTNORepinephrine" to mean epinephrine. Damn, I may be NOTNOTDumber as I thought. Or does the logical operator "NOTNOT"Dumber return MOREDumber? Noooo. It returns as dumb but NOT dumber. Whew.
I've stumbled across some valuable info I wasn't directly searching for. I've had a persistent problem with logical operators of the brain type. I swear, Thu, a few of the doctors I visited impressed me as being incompetently dumb. Prior to seeking medical help with my newly dxed ADHD, 5 or 7 years or so, I viewed medical doctors with respect. I opinioned that it took brains, scholarship, 4 years of college, followed by another 8 years of medical school and internship (or is it more?) to make the grade. The job requires the ability to call on demand a gadzillion details and apply them correctly. Or someone dies. Heavy duty responsibility.
I got the missing link that caused me to over draw my bozo doctor conclusion. I was reading one of the many research reports when I saw it. Doctors do NOT want us as patients. Many doctors perceive us as far more trouble than what we are worth. They know amphetamines are most effective for managing ADHD. They also know that regardless of patient need, they cannot write too many amphetamine prescriptions or dare not exceed the recommended maximum dose. They'll have the FDA, DEA, FBI and CIA on their backs scrutinizing every more they make.
Another factor the research report noted was, especially adult ADHD patients do not respond nearly as well to mental disorder medications as do the patients with physical below the neck illnesses. We make doctors look bad. We make them look incompetent. I flamed two or three doctors right proper as I stormed out. Now I know their response I couldn't see. "Whew, good riddance."
What is motivating me to put so much effort into my research? Mistakes I made along the way to ADHD management.
I did not respond well to meds at the get-go. After I found a good psychiatrist and got the meds tweaked pretty well I did pretty well. Then I hit a plateau that kept me from more progress. It was then I realized that I needed CBT. The meds were doing their job. Teaching me the good habits and skills that ADHD prevented me from developing isn't in the medication's job description. I benefited nicely from CBT. Everyday I habitually use the principles learned. I'm not consciously controlling the skillset anymore than I'm consciously controlling my finger movements as I type now.
All along I continued to have a horrible time in the evenings after the meds wore off. I kept looking for a solution along the lines of CBT but found nothing. The ADHD rebound I experience has got to be among the worst. I lose control my thinking processes. The mental chaos does cause me anxiety. Anxiety does not precede the chaos. I think it a rational response to loss of control. Ever lose control of your car on black ice? I have on two occasions. Each case. "Oh, poop, that tree is in my path." The tree isn't moving and I can't control the direction or slow the speed of my car turned "Bob-sled." Hmn, fairly funny, pun, eh? I felt anxious worrying over how much damage I am about to sustain. Each case, I missed the tree. Both man and machine drove off unscathed. At about .5 MPH. I'll convert for you. About 0.8 km/h. Scared poopless.
Guanfacine is turning the trick for me. The lesson learned. Patient implementation of cognitive behavioral therapy requires the mental functions that ADHD deprives. CBT is worthless until after the meds are in place and stabilized. I tried my hardest to find a non-medical remedy but found nothing with lasting efficacy. The medical solution, guanfacine, is working. There are no work-arounds available until after the biology based problem is under control.
I never would have gotten a guanfacine prescription if I had not done my homework.
I'm sure the research I'm now doing will pay off in the not too distant future. This ADHD bug along with its comorbids seems to have a knack for getting loose on me after I get them nailed down tight.
Psychotropic meds cause more neurotransmitter to enter the synapse or cause the neurotransmitter to remain in the synapse longer and in many cases, the meds affect both actions.
Why they help.
Key point: The neuron will not fire an action potential until the sum of all of its synaptic electrical charges (potentials) at any one moment equals or exceeds its threshold.
Each neuron is said to be "all or nothing." Either the neuron fires or it doesn't fire. The postsynaptic neuron fires when the sum total of all its postsynaptic receptors put-through charges equal or exceed the neuron's threshold. The neuron "spikes" on >= threshold and outputs its neurotransmitter. Each charge dissipates rapidly on synaptic neurotransmitter (signal) termination. The input is lost if the neurotransmittor signal terminates before the postsynaptic neuron reaches its threshold.
Therefore, if we get more neurotransmitter into the synapse and we get it to stay in the synapse longer, we stand a much better chance that the postsynaptic neuron threshold will be reached and fires just like we want it too.
Different medications work on different mechanisms in the synapse and in the neurons on both sides of the synapse. The more powerful meds, such as amphetamines, work on many mechanisms causing a cascading increase in both quantity and time of the effected neurotransmitters in the synapse.
The above is a pretty accurate layman's description.
How does it help me?
If we can add more synapses between each neuron to neuron connection, we increase the odds that the postsynaptic neuron threshold will be reached and fire its output.
It could be that psychotropic meds are over-boosting each synapse to compensate for the lack of synapses in an under developed system. Many top shelf experts subscribe to the "developmental delay" theory to explain ADHD. I lean heavily toward that opinion. Kids can grow out of ADHD. Adults can too with medication and therapy and time. Severity can monkey wrench some into a life-time with ADHD. For the latter, life-long medication can manage the disorder well enough so they function satisfactorily.
Please, note, everything I've written including what I've deemed "accurate" is grossly over simplified. I tried going from the micro view to the macro view. I take one step up into the macro and I lose everything I think I know into an unbelieveable, heck, unimagineable complexity of the CPU we can our "brain." Wow. I'm done with it for the sake of keeping the little sanity I possess.
Bravo Bob! I especially like what you said about the use of meds and "irrationally rejecting pyschiatric care". Both improve "quality of life", and that of course, is a very good thing. Some people don't believe in the use of meds, but I look at it this way. There are many disorders/illnesses, some more serious than attention defficit, some less, some fatal, that meds, under a Dr's care, are used to treat. They greatly improve the "quality of life" for a lot of those people, in some cases, keep them alive. I believe, ADD/ADHD should be treated the same way. I, for one, feel much more alive than ever, and now have a more positive outlook on life, following diagnosis, and treatment(with meds and shrink). The meds are helping me improve my relationship with my wife. For example, COMMUNICATION, which is the biggest thing I can think of in a marriage, or any partnership. I like seeing the shrink because it's "maintenance" and "preventative maintenance" , for me. I will, guess I already have, work on getting my "A.D.H.D." in ADHD. The best part is, I won't ever model the negativity associated with ADHD, to my son, and I can look out for signs, and symptoms, if he is inflicted with the disorder as well. Plus, I'll know what to do and expect. I wish I had been diagnosed as a kid, I could have been so much more!( I'll get over it) The more I educate myself in ADHD, and follow through with ALL avaialble treatment, the better for myself and my family!
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