View Full Version : Executive Dysfunction in children and adolescants with ADHD, Autism, Bipolar, etc.


Abi
01-08-14, 08:16 PM
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/

Tulip7171
01-08-14, 09:13 PM
Thank you!

I've been looking into EF dysfunction the last couple of days because I wonder if my issues are all ADHD, maybe some autism spectrum issues or anxiety.

Correct me if I misunderstood, but did it say that anxiety does not seem to disrupt EF? That would help me narrow things down a bit.

Abi
01-08-14, 09:15 PM
Yes, that's correct.

mildadhd
01-08-14, 09:55 PM
...Executive dysfunction indicates some malfunction in the circuits that connect the sub-cortical areas with the frontal lobes (Rosenblatt & Hopkins, 2006). Both genetic and environmental factors can interfere with ES efficacy.


See OP link (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/)



i!i

Amtram
01-09-14, 02:11 PM
Executive dysfunction, I hope, will eventually become its own category. Then again, I'm very much in favor of much more specificity in diagnosis and treatment.

The thing with EF disorders is that there are two things to consider - brain function and structure, and environmental structure. Whatever is not working correctly in the brain is going to have a wide range of effect. An EF disorder can be relatively minor and correctable with a home and school structure that teaches skills to compensate; it can be sometimes addressed with medications that ameliorate the signalling imbalances in the brain, allowing a person to function within a normally-structured environment; it can be severe enough to require both; it can be so severe that it cannot be overcome.

However, it can be self-perpetuating. Without the emotional support and teaching of adults around a child, not only will the behaviors continue (because the child doesn't learn them as intuitively as non-impaired children do) but the continued cycle of failure will discourage the child from learning how to self-regulate.

Unfortunately, we seem to have a dichotomy of opinion, with one side saying these problems are made up and correctable with, say, corporal punishment - and another saying that we can fix things with medication. Neither side is correct. However, as you can see from this meta-analysis, there's been a lot of scientific focus on the molecular roots of EF dysfunction, and much less on behavior modification strategies.

Part of it comes from having to address EF dysfunction as part of a larger collection of symptoms. And it makes sense, in a way, because the psychological strategies that work with an ADHD child are definitely not going to apply just as well to one with FASD. Still, with a better understanding of EF in the first place, it's a step forward in addressing it more effectively within all the conditions that exhibit executive function deficits.

daveddd
01-09-14, 02:22 PM
Thank you!

I've been looking into EF dysfunction the last couple of days because I wonder if my issues are all ADHD, maybe some autism spectrum issues or anxiety.

Correct me if I misunderstood, but did it say that anxiety does not seem to disrupt EF? That would help me narrow things down a bit.

the relationship between anxiety and depression generally is thought to go in the other direction

Abi
01-09-14, 03:17 PM
Job market looking exceeding bleak for sufferers of ADHD and other Executive Functioning impairing conditions:

http://www.psychologytoday.com/blog/radical-teaching/201104/whose-children-will-get-the-best-jobs-in-the-21st-century

mildadhd
01-10-14, 01:16 AM
the relationship between anxiety and depression generally is thought to go in the other direction


I think we can also experience anxiety and depression during early development, from the ground up.

Especially before the age of 4.

When everything is emotionally bigger.

As we get older, top down, becomes cognitively bigger.

I think ,moderate ADD impairment, occurs before the age of 4.

At birth, the loop begins from the ground up (subcortical), not the top down (cortical).

Top down executive control becomes big as we age and reach adulthood.

But we all have ADD before the age 7-10 for sure.

Making early ground up development the primary focus, when discussing primary impairment.


Executive control is definitely impaired, in ADD.

But what effected the executive control, resulting in impairment?








Laymans

mildadhd
01-10-14, 11:36 PM
the circuits that connect the sub-cortical areas with the frontal lobes (Rosenblatt & Hopkins, 2006).


The lower subcortical areas connect to the higher cortical areas.

Prefrontal cortex equals higher cortical areas.

What equals the lower subcortical areas?

Brain imaging research does a good job of measuring the higher cognitive function.

And has helped tremendously in developing earlier psychological hypothesis.

Although, if I understand correctly people are unable to move during brain imaging, and imaging does not measure the subcortical primary emotions very well.

Other methods of measurement must also be considered, along with brain imaging, to understand the connections between the subcortical and cortical areas, before, and during natural early childhood development of executive systems.




Laymans

EmilyRay42
01-11-14, 12:47 AM
This explains why, when I was given the Neuroleptic Haldol I became more anxious not less! I really need to stop reading and learning. All it does is raises my level of frustration at the incompetent medical care I have received in the past three years.

Abi
01-11-14, 01:44 AM
Odd. Haldol makes me very Zen, but completely stupid and incompetent.

I thought Depakote was zombifying but Haldol was at a whole different level.

Oddly, my ignorant 70 year old state shrink said that Haldol would "clear my head" and improve cognitive function.

Two medications that DID help with the above have been the NDRI Wellbutrin, which I still take, and the ATYPICAL neuroleptic Risperdal, which I hat to stop due to intolerable physical side effects (extreme weight gain, water retention/oedema and muscle weakness.)

EmilyRay42
01-11-14, 02:32 AM
I only took it for two days and developed Neuroleptic Malignant Syndrome. That may be why I was getting more anxious and not less. I was also on Compezine at the same time and they work synergistically on the same area of the brain. I should have never been given it because I was on a high dose of a diuretic that kept me in a constant state of dehydration which increases the risk of Neuroleptic Malignant Syndrome. It was a miserable experience I wouldn't want anyone to go through. The Doctors never admitted it happened and believed I was faking my symptoms! I only found out later that if I would have continued the Haldol I could have died.

mildadhd
01-11-14, 01:10 PM
This explains why, when I was given the Neuroleptic Haldol I became more anxious not less! I really need to stop reading and learning. All it does is raises my level of frustration at the incompetent medical care I have received in the past three years.

Excuse my ignorance, are you saying you where prescribed Neuroleptic Hadol to treat executive impairment?




Peripherals

Abi
01-11-14, 01:43 PM
Excuse my ignorance, are you saying you where prescribed Neuroleptic Hadol to treat executive impairment?




Peripherals

Can't speak to her; but I was.

My psych is 70 years old and very stupid, works in the state sector, so don't take his prescription opinions very seriously.

meadd823
01-11-14, 02:29 PM
I was wondering what any of this has to do with the topic - darned ADDers can't stay on topic for squat - Now what were we talking about ???


Oh yeah the psychiatric trash can catch all good ole EF - one of my unfavorite favorite topics. . .. some thing like that

Any way allow me to direct attention to the initial source

A Review of Executive Function Deficits and Pharmacological Management in Children and Adolescents (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/)


Abundant literature was found on the nature of the ES and the executive dysfunctions in most psychiatric disorders in children and adolescents, but not so much on the use of medication. EF deficits were found to be more consistent in disorders such as ADHD, ASD and FASD than in the other disorders but were not specific enough for use as clinical markers for those disorder

Existing literature indicates that EF deficits underlie most psychiatric disorders in children and adolescents. However, there are so many executive functions linked to so many activities and circuits in the brain that it is hard to quantify them in a particular disorder for use as specific markers for that disorder.


I would say that the frontal lobes are a dysfunctional manifestation in and of themselves - any thing that weak with as many errors in functioning as to be the cause of just about all psychiatric disorders should not exist in the first place.

My point is they blame every thing on the frontal lobes with little or no consideration to the rest of the brain which has by the way been around a lot longer and is adaptively possed by more mammalian life forms.


Research focusing on how observable symptoms relate to specific EF deficits has important implications for future psychopharmacological interventions in this area by elucidating the neural substrates and pathways which underpin symptomatology


The word monoculture comes to mind . . . . I feel like human are expected to march to the same beat of the same drum as if that is necessary for our future when I question that very future in light of those societies in days past who insisted that every one think and act alike - I think we called them dictatorships.

I am not against medication by any means but I am against the expectation that we all fall into some imaginary line of social expectations without question as the the reasoning behind natures insistence to bestow the curse of neurodiversity for a large percentage of the human population.

One or two percent we have a genetic screw up five to eight percent we have diversity which may or may not be relevant to the future in which no one has a knowledge of despite many pretending to in the preceding article which asserts EF to being able to deal with changing situations - Forgetting that the constantly confused are rarely if ever bothered by changing situations not to mention that despite the desire to cram us all into one nice neat little box not all ADDers are alike nor do we react to all situation in like manner.

Some ADDers are thrown off by changing environments while other ADDers are bored by the overly predictable.

Okay my computer time is officially up gotta run and do some thing more productive although less pleasant - laundry comes to mind - dirty uniforms need undirtying :rolleyes:




. . . ..

mildadhd
01-11-14, 02:53 PM
Executive dysfunction has been linked to underarousal of dopamine systems.

How does overarousal of dopamine systems, in people who suffer from schizophrenia, also, result in executive impairment?

I am not doubting that people with symptoms of schizophrenia, may have executive dysfunction.

I am curious to know how overarousal of dopamine system, also, can result in executive dysfunction?

Are the same executive systems involved, in all cases of executive dysfunction?









Peripherals Laymans

daveddd
01-11-14, 02:54 PM
If I understand correctly, people with schizophrenia show executive impairment?

How does overarousal of dopamine systems, also, result in executive impairment?

I am not doubting that people with symptoms of schizophrenia, may have executive dysfunction.

I am curious to know how overarousal of dopamine system, also, can result in executive dysfunction?









Peripherals

id have to question the directionality of the relationship

Abi
01-11-14, 03:02 PM
M,

There are dopamine receptors at different sites of the brain.

Someone with, say, comorbid Schiz + ADHD or someone with Bipolar like myself may have a dopamine excess at some parts of the brain (causing mania) and a dopamine deficits in other parts (causing depression).

It's not uncommon to see a patient with schizophrenia combined with ADHD to be taking say, Haldol (DA antagonist) and say, Dexedrine (DA agonist) concomitantly.

I myself take Wellbutrin (DA agonist) and have at times concurrently taken Risperdal or Haldol (DA antagonists)

A few medications (Abilify comes to mind) act as DA agonists at some sites in the brain and DA antagonists at others.

daveddd
01-11-14, 03:04 PM
M,

There are dopamine receptors at different sites of the brain.

Someone with, say, comorbid Schiz + ADHD or someone with Bipolar like myself may have a dopamine excess at some parts of the brain and a dopamine deficits in other parts.

It's not uncommon to see a patient with schizophrenia combined with ADHD to be taking saym Haldol (DA antagonist) and say, Dexedrine (DA agonist).

I myself take Wellbutrin (DA agonist) and have at times taken Risperdal or Haldol (DA antagonists)

A few medications (Abilify comes to mind) act as DA agonists at some sites in the brain and DA antagonists at others.

certain anti psychotics are now also being shown effective for adhd

mildadhd
01-11-14, 03:16 PM
Thanks, I am interested learning more.

Side Note: The person I am working for gave me the option to come into work today, when I want.

Presently the day is half gone, and I better get going, (I hate to admit it but sometimes supervision does seem to help.)

My heart goes out to all people suffering in these frustrating complex predicaments.





Peripherals

Amtram
01-11-14, 04:30 PM
I would say that the frontal lobes are a dysfunctional manifestation in and of themselves - any thing that weak with as many errors in functioning as to be the cause of just about all psychiatric disorders should not exist in the first place.

My point is they blame every thing on the frontal lobes with little or no consideration to the rest of the brain which has by the way been around a lot longer and is adaptively possed by more mammalian life forms.

. . . ..

From the text:

The ES is mediated by various networks in the frontal, parietal and occipital cortices, the thalamus and the cerebellum (Jurado & Roselli, 2007 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b31-ccap21_3p0223)). It is linked through a series of circuits connecting every region of the central nervous system. The circuits originate in the dorsolateral prefrontal cortex (PFC) / orbitofrontal cortex (OFC), project through the striatum, synapse at the level of the globus pallidus, substrantia nigra and the thalamus and finaly return to the PFC forming closed loops (Narushima, Paradiso, Moser, Jorge, & Robinson, 2007 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b43-ccap21_3p0223)). Each circuit regulates specific functions. The circuit that is most responsible for coordinating EF is located primarily in the frontal lobe. Functional imaging studies have implicated the PFC as the primary site of cortical activation during tasks involving EF (Elliott, 2003 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b13-ccap21_3p0223)).

The executive system is not being considered as existing solely in the frontal lobes by these researchers. It's the primary source of executive function, but the system itself is comprised of multiple brain areas.

mildadhd
01-12-14, 09:30 PM
The mesocortical pathway (http://en.wikipedia.org/wiki/Mesocortical_pathway) is a dopaminergic pathway that connects the ventral tegmentum to the cerebral cortex, in particular the frontal lobes. It is one of the four major dopamine pathways in the brain. It is essential to the normal cognitive function of the dorsolateral prefrontal cortex (part of the frontal lobe), and is thought to be involved in cognitive control, motivation, and emotional response.[1][2]

This pathway may be the brain system that is abnormal or functioning abnormally in psychoses, such as schizophrenia.[3] It is thought to be associated with the negative symptoms of schizophrenia, which include avolition, alogia and flat affect. This pathway is closely associated with the mesolimbic pathway, which is also known as the mesolimbic reward pathway.



The mesolimbic pathway (http://en.wikipedia.org/wiki/Mesolimbic_pathway) is a dopaminergic pathway in the brain. The pathway begins in the ventral tegmental area of the midbrain and connects to the limbic system via the nucleus accumbens, the amygdala, and the hippocampus as well as to the medial prefrontal cortex. The mesolimbic dopamine system is widely believed to be a "reward" pathway, but that hypothesis is not universally accepted.[1]

The nigrostriatal pathway (http://en.wikipedia.org/wiki/Nigrostriatal_pathway) is a dopaminergic pathway that connects the substantia nigra with the striatum. It is one of the four major dopamine pathways in the brain, and is particularly involved in the production of movement, as part of a system called the basal ganglia motor loop.


The tuberoinfundibular pathway (http://en.wikipedia.org/wiki/Tuberoinfundibular_pathway) refers to a population of dopamine neurons in the arcuate nucleus of the mediobasal hypothalamus (the 'tuberal region') that project to the median eminence (the 'infundibular region'). It is one of the four major dopamine pathways in the brain. Dopamine released at this site regulates the secretion of prolactin from the anterior pituitary gland.




All the dopamine pathways project from the "pre executive" subcortical areas.

Mature cortical areas do "mediate" subcortical areas.

But dopamine pathways "originate" from the ground up subcortical areas, during early development.









Peripherals

meadd823
01-18-14, 01:49 AM
From the text:

The ES is mediated by various networks in the frontal, parietal and occipital cortices, the thalamus and the cerebellum (Jurado & Roselli, 2007 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b31-ccap21_3p0223)). It is linked through a series of circuits connecting every region of the central nervous system. The circuits originate in the dorsolateral prefrontal cortex (PFC) / orbitofrontal cortex (OFC), project through the striatum, synapse at the level of the globus pallidus, substrantia nigra and the thalamus and finaly return to the PFC forming closed loops (Narushima, Paradiso, Moser, Jorge, & Robinson, 2007 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b43-ccap21_3p0223)). Each circuit regulates specific functions. The circuit that is most responsible for coordinating EF is located primarily in the frontal lobe. Functional imaging studies have implicated the PFC as the primary site of cortical activation during tasks involving EF (Elliott, 2003 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413474/#b13-ccap21_3p0223)).

The executive system is not being considered as existing solely in the frontal lobes by these researchers. It's the primary source of executive function, but the system itself is comprised of multiple brain areas.

Underlining added by me - if the frontal lobes are the primary source of executive function and the functioning does not function worth a crap then the primary system is not operating worth a crap one way or the other.

Executive function , executive system functioning are basically meanness terminology referring to various parts of the brain so people can present as if they know wtf they are talking about when they really have not much of a clue. . .

What this is saying is - the problem could be in any number of these fifteen brain areas or in the way they relate to one another but we really are flat out clueless as to what the exact the problem is - :doh:

Simplifying is not the same thing as failure to understand!

Amtram
01-18-14, 12:16 PM
Actually, no, it's not saying that. It's saying that there is a network of neuronal pathways that are interdependent in different ways, and that while the Prefrontal Cortex initiates most of the actions in the Executive System, it is not the only part that is involved in the overall functioning of the system.

While we don't know everything, there is enough understanding of brain function to build on - and we know that by learning the function of individual brain areas and being able to measure electrical connectivity we can better understand what part of the Executive System might be functioning improperly.

The brain is the most complex organ in the body. Oversimplification does lead to wrong answers. The loops being discussed in the quoted paragraph are similar to most other functions in the brain, and like any electrical system, can function improperly if there's a broken connection anywhere else in the loop. The PFC sends out a signal, that signal travels through a series of brain areas using a neuronal pathway, and then that signal returns to the PFC. Any break or weakness along that pathway will interrupt the signal and impair executive functioning in some way. Therefore, even with a PFC that is performing properly, a person with EF dysfunction can still have that dysfunction. The problem can be in one of the other components of the loop. Therefore, saying that it's all in the PFC is incorrect, and claiming that all the scientists are talking about is the PFC is also incorrect. It is not a matter of conceit.

Amtram
01-18-14, 01:54 PM
BTW, we have an older thread on here, http://www.addforums.com/forums/showthread.php?t=128524, which started off with a description of traumatic injury to the prefrontal cortex. If only the PFC were involved in executive function, we'd look a lot more like the patient in the description than ourselves. An interruption somewhere in the neuronal loop affects only a subset of the symptoms this patient experienced.

Amtram
01-19-14, 11:15 AM
BTW, a broken link in the loop doesn't render the entire loop completely nonfunctional. Just as with, say, highway construction, a blockage in the direct route can be partially compensated for by an alternate route. That alternate route, naturally, is going to slow the process down at best. At worst, the additional connections associated with the alternate route will result in the signal getting lost or going to the wrong places.

To some degree, some of these alternate routes can be refined by learning strategies. Nothing will fix the break, but sometimes knowing where the problem is and designing a therapeutic strategy to address it can help a person with executive dysfunction learn to lessen the loss of signal by learning how to direct it more consciously.

Like any form of learning, this can possibly cause some neuronal migration that shortens the "alternate route." Obviously, there's no guarantee because of the number of possible causes that we can't ethically or practically investigate, and the diversity of human brains in general. It also requires a good deal of conscious thought and directed therapies to teach yourself to "take the shortest alternate route." Even once a successful strategy is learned, it doesn't necessarily become automatic.