Here is a long article again documenting the reality of the ADHD diagnosis. I was slightly surprised to see in the final paragraph how much traumatic brain injury can mimic ADHD. Or, does it in fact, produce ADHD? I think not; it is a different disorder with similar symptoms.
I’ve had many blows to the head, but only one real concussion. That was due to a sucker punch. The real fight was only after I recovered some hours later. It was payback time. However, this is all irrelevant, because I clearly exhibited ADHD symptoms starting at least in the fourth grade and had few if any blows to the head before that and none serious.
I believe ADHD is not just one end of a spectrum, but is separate and distinct. I also believe that at least for some of us there’s delayed maturation of the developing brain, which can be partly corrected with time and improved by medication, which apparently can do more than just treat symptoms. However, I can’t tell if this article supports or refute that idea.
I think this is a good article, but it is too long, too detailed, and too complicated for me to easily read or to fully understand. I was very tempted to just scan it. In fact, I did.
For the scientific minded, the article: (Or skip it. Just scroll down for some more good stuff.)
The pathology of ADHD is not clear. Psychostimulants (which facilitate dopamine release) and noradrenergic tricyclics used to treat this condition have led to speculation that certain brain areas related to attention are deficient in neural transmission. PET scan imaging indicates that methylphenidate acts to increase dopamine.  The neurotransmitters dopamine and norepinephrine have been associated with ADHD.
The underlying brain regions predominantly thought to be involved are frontal and prefrontal; the parietal lobe and cerebellum may also be involved. In one functional MRI study, children with ADHD who performed response-inhibition tasks were reported to have differing activation in frontostriatal areas compared with healthy controls. A 2010 study again indicated the presence of frontostriatal malfunctioning in the etiology of ADHD.  Although ADHD has been associated with structural and functional alterations in the frontostriatal circuitry, recent studies have further demonstrated changes just outside that region and more specifically in the cerebellum and the parietal lobes.  Another study using proton magnetic spectroscopy demonstrated right prefrontal neurochemical changes in adolescents with ADHD. 
Work by Sobel et al has demonstrated deformations in the basal ganglia nuclei (caudate, putamen, globus pallidus) in children with ADHD. The more prominent the deformations, the greater the severity of symptoms. Furthermore, Sobel et al have shown that stimulants may normalize the deformations. 
Adults with ADHD also have been reported to have deficits in anterior cingulate activation while performing similar tasks.
In a longitudinal analysis, Shaw et al used 389 neuroanatomic MRI images to compare 193 typically developing children with varying levels of symptoms of hyperactivity and impulsivity (measured with the Conners’ Parent Rating Scale) with 197 children with ADHD (using 337 imaging scans).  Children with higher levels of hyperactivity/impulsivity had a slower rate of cortical thinning. This was most notable in prefrontal cortical regions, bilaterally in the middle frontal/premotor gyri, extending down the medial prefrontal wall to the anterior cingulate. It was also noted in the orbitofrontal cortex and the right inferior frontal gyrus. Slower cortical thinning during adolescence is characteristic of ADHD and provides neurobiological evidence for dimensionality.
A PET scan study by Volkow et al revealed that in adults with ADHD, depressed dopamine activity in caudate and preliminary evidence in limbic regions was associated with inattention and enhanced reinforcing responses to intravenous methylphenidate. This concludes that dopamine dysfunction may be involved with symptoms of inattention but may also contribute to substance abuse comorbidity. 
Individuals with ADHD have inhibition impairment, which is difficulty stopping their responses. 
According to a study of young children, there is evidence of early brain structural chages in pre-schoolers with ADHD. Researchers used high resolution anatomical (MPRAGE) images and cognitive and behavioral measures in a cohort of 90 medication-naïve preschoolers, aged 4–5 years (52 with ADHD, 38 controls; 64.4% boys). Results show reductions in bilateral frontal, parietal, and temporal lobe gray matter volumes in children with ADHD relative to typically developing children. The largest effect sizes were noted for right frontal and left temporal lobe volumes. Examination of frontal lobe sub-regions revelated that the largest between group effect sizes were evident in the left orbitofrontal cortex, left primary motor cortex (M1), and left supplementary motor complex (SMC). ADHD-related reductions in specific sub-regions (left prefrontal, left premotor, left frontal eye field, left M1, and right SMC) were significantly correlated with symptom severity, such that higher ratings of hyperactive/impulsive symptoms were associated with reduced cortical volumes. 
Narad et al. explored the relationship between traumatic brain injury (TBI) in children and development of secondary attention-deficit/hyperactivity disorder (SADHD).  They looked at concurrent cohort/prospective studies of children aged 3 to 7 years who were hospitalized overnight for TBI or orthopedic injury (OI; used as control group). A total of 187 children and adolescents were included in the analyses: 81 in the TBI group and 106 in the OI group. According to the results, early childhood TBI was associated with increased risk for SADHD. This finding supports the need for post-injury monitoring for attention problems. Consideration of factors that may interact with injury characteristics, such as family functioning, will be important in planning clinical follow-up of children with TBI.”
Quote O the Day:
“Happiness is clear nasal passages.”
from a man who had a cold.
Always love the pictures you include with the posts, Doug! Where do you get them?
I like the second one, asking if epilepsy is made-up too. When someone starts saying that people with ADHD just need to focus, I feel like saying “Yeah, if only those damned parkinson patients would stop shaking, dammit! Half their problems would be solved!”.
Vanillas don’t seem to get that focus very much has to do with neurotransmitters. Same as muscle coordination, that they seem willing to accept as something neurological, they take the aiming of your focus for granted.
People have a hard time accepting mental disorders – even a “simple” clinical depression – because it’s not like a broken leg, but I’ve come up with an analogy to a broken leg that might help clear things up with those people:
if you break a leg, you can’t see it either (unless it’s a compound fracture). For some reason, if you have immense pain after falling down, people tell you to go to a hospital to get checked out because it might be broken. When you suffer through a psychological trauma, people have a hard time believing something like depression could develop. They think “I wouldn’t get depressed” and don’t seem to factor in that a lot of people fall downstairs withouth breaking a bone, while others break easily. They just go “Just pull it through” but they don’t tell a person who fell down the stairs to “walk it off”. Why? Let them mull this over.
When the leg is broken, just like with a clinical depression, you don’t NEED medical attention. You can heal alone. Of course, like with depression, you’ll end your life limping because it didn’t heal properly. If you have “bad luck”, without treatment, you’ll die from complications – both from a broken leg and from clinical depression (suicide, self-harm).
If you get your broken leg treated, you get the bone set and you get a cast. Nobody expects you to put your full weight on the bad leg again. It’s acceptable to go on sick leave, to take the elevator instead of the stairs. With a depression, normal reaction is “Well, but you’re taking meds now, you should be fine and be able to do everything!”. Why? If you would not expect a leg to heal as soon as you put on a cast, why would you expect the psyche to be able to do that? Heck, even antibiotics don’t work immediately.
You also need physical therapy after a broken leg, because the use of the leg was compromised for so long. And despite how often people will try to sound smart and comment on a news article they read about scientists showing that crosswords can train the mind like a muscle; no matter, for some reason, they expect a person to just pop out of clinical depression. Ask them why. Ask them to mull it over.
Finally, when the cast is off, along with the physical therapy, you have to take it easy. The leg is fully functioning but still weak. Even professional athletes have to take it easy with training after such an incident. Why would anyone expect someone who recovered from depression to be their old self immediately? Let them mull it over.
good examples. for some reason people dont like to accept problems like ADHD or depression. not clear why.
your comment reminds me of when i broke my leg and the coach who was a Christian Scientist, told to me to “just run it off.” didnt work.
the images are just off the net, google ADHDfunny or etc.
thank you for commenting
oh man i loved this post.
1. re: neurotransmitters associated with ADHD: what about serotonin? what if the neurotransmitters associated with ADHD aren’t limited to just dopamine and norepinephrine? asking this question because a big part of ADHD that is often overlooked is emotional self-regulation.
note: my background isn’t in biopsych or psychopharm so it’s safe to say i’m well out of my domain here.
2. i think they’re also finding that the basal ganglia is different in people with ADHD. that definitely could explain some of the emotional dysfunctions and possibly poor coordination and clumsiness seen in children (& let’s face it–adults).
(sidenote: i was writing down notes/thoughts as i was reading through your lit review and….. just got to where the basal ganglia got addressed in your article. typical me, not finishing reading/listening before i say something. if i read that first, i wouldn’t have needed to write point #2 but whatever i already wrote it so i just left it)
3. i didn’t know that SADHD was something that got acknowledged in the literature–i always suspected it being a thing but am glad to see that somebody out there is exploring it even further. i 100% believe that ADHD (or at least its associataed symptomology) can be developed without one necessarily having to be born with it (i.e. sleep disorders, TBIs, drug use). The current diagnostic methodology’s dependence on childhood symptoms does not take these things into consideration at all, which I believe is a really, really big problem.
ADHD sucks man. i think that our diagnostic methodology is way overdue for an update and the research needs to focus more on adults with the disorder, not just mostly children. there isn’t enough emphasis on dysfunctional emotional/affective self-regulation. we’ve basically been using the same psychopharmacological approach since the 70’s. and damn it why are we still calling it ADHD when attention is just ONE of the disorder’s symptoms? it’s an executive functioning disorder.
man, i really need to get back to work. good talk
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glad you liked it. there’s probably different flavors of ADHD and possibly some involve serotonin, but i’ve never seen or heard of those meds (SSRI) helping ADHD. clearly we need better classification and diagnoses. and pretty clear the cerebellum and basal ganglia are involved along with frontal lobe. i’m doubtful about the other causes, and about not starting in childhood, but brain injury can mimic (cause?) it.
i always appreciate your comments. not ready to tackle dragon again yet, too distracted.
“ADHD sucks man. i think that our diagnostic methodology is way overdue for an update and the research needs to focus more on adults with the disorder, not just mostly children. ”
Very good point! I think I can think back to my childhood and pinpoint things that had to do with ADHD. But even if someone back then had asked me what was wrong, I simple didn’t have enough experience and vocabulary to explain it.
Nowadays, knowing that ADHD is related to chemichals that deliver information to the nervous system (neurotransmitters), I have no problem recognizing and rationalizing certain things. Exampe: A colleague 10 feet away said something that I didn’t understand. I asked her to repeat it, and just as she was repeating it, an apprentice 2 feet away from me started mumbling a reply softly, because she thought I was talking to her. What happened was, I couldn’t hear my colleague because my brain just couldn’t “figure out” which message to carry. Some sounds – like background noise – just become as loud as the more important sounds in the situation, no matter how soft the background noise is.
It does tend to dissapear with habbit in reocurring situations. When I started playing the guitar, the sound of the pick scraping against the strings was unbelievably loud to my ears, muffling the sound of the guitar. With time, this feeling went away (my brain figured out, through lots of effort, which of the two sounds it has to focus on). Although even better for me is playing the electric guitar with headphones on: even more muffling of the unwanted sound from the pick action on the strings.
Now, ask a child what’s its problem, and it will say it can’t hear, and you probably end up putting the child through hearing tests. Some children have a tooth ache and when you ask them what’s wrong, they can’t identify the issue and tell you they have a headache (because the teeth are inside the head). Or they confuse a sore throat with a tummy ache. It defenitely makes children more challenging to diagnose and I support your oppinion: I think we could take long strides in the investigation of ADHD in children by interviewing and testing adults with ADHD, because they mechanisms – as I recall them from my childhood, when I was undiagnosed – seem to be pretty much the same.
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