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.