The Pathophysiology of Adhd

Research on children with ADHD has shown a general reduction of brain volume, but with a proportionally greater reduction in the volume of the left-sided prefrontal cortex. These findings suggest that the core ADHD features of inattention, hyperactivity, and impulsivity may reflect frontal lobe dysfunction, but other brain regions particularly the cerebellum have also been implicated. 88] Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research not diagnostic purposes. [89] A 2005 review of published studies involving neuroimaging, neuropsychological genetics, and neurochemistry found converging lines of evidence to suggest that four connected frontostriatal regions play a role in the pathophysiology of ADHD: The lateral prefrontal cortex, dorsal anterior cingulate cortex, caudate, and putamen. 90] In one study a delay in development of certain brain structures by an average of three years occurred in ADHD elementary school aged patients. The delay was most prominent in the frontal cortex and temporal lobe, which are believed to be responsible for the ability to control and focus thinking. In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterizes ADHD.

It should be noted that stimulant medication itself may affect growth factors of the central nervous system. [92] The same laboratory had previously found involvement of the “7-repeat” variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement. 93] Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),[94] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. [95][96] A study by the U. S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain’s ability to roduce neurotransmitters like dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine (hypodopaminergia) across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor.

In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to “childhood learning problems” in healthy subjects as well. [97] One interpretation of dopamine pathway tracers is that the biochemical “reward” mechanism works for those with ADHD only when the task performed is inherently motivating; low levels of dopamine raise the threshold at which someone can maintain focus on a task which is otherwise boring. [98] Neuroimaging studies also found that neurotransmitters level (e. . dopamine and serotonin) in the synaptic cleft goes down during depression. [99][100] A 1990 PET scan study by Alan J. Zametkin et al. found that global cerebral glucose metabolism was 8% lower in medication-naive adults who had been hyperactive since childhood. [101] Further studies found that chronic stimulant treatment had little effect on global glucose metabolism,[102] a 1993 study in girls failed to find a decreased global glucose metabolism, but found significant differences in glucose metabolism in 6 specific regions of the brains of ADHD girls as compared to control subjects.

The study also found that differences in one specific region of the frontal lobe were statistically correlated with symptom severity. [103] A further study in 1997 also failed to find global differences in glucose metabolism, but similarly found differences in glucose normalization in specific regions of the brain. The 1997 study also noted that their findings were somewhat different than those in the 1993 study, and concluded that sexual maturation may have played a role in this discrepancy. 104] The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results. [105][106][107] Critics, such as Jonathan Leo and David Cohen, who reject the characterization of ADHD as a disorder, contend that the controls for stimulant medication usage were inadequate in some lobar volumetric studies which makes it impossible to determine whether ADHD itself or psychotropic medication used to treat ADHD is responsible for the decreased thickness observed[108] in certain brain regions.

While the main study in question used age-matched controls, it did not provide information on height and weight of the subjects. These variables it has been argued could account for the regional brain size differences rather than ADHD itself. [109][110] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology. [109] Diagnosis

ADHD is diagnosed via a psychiatric assessment; to rule out other potential causes or comorbidities, physical examination, radiological imaging, and laboratory tests may be used. [111] In North America, the DSM-IV criteria are often the basis for a diagnosis, while European countries usually use the ICD-10. If the DSM-IV criteria are used, rather than the ICD-10, a diagnosis of ADHD is 3–4 times more likely. [13] Factors other than those within the DSM or ICD however have been found to affect the diagnosis in clinical practice.

A child’s social and school environment as well as academic pressures at school are likely to be of influence. [112] Many of the symptoms of ADHD occur from time to time in everyone; in patients with ADHD, the frequency of these symptoms is greater and patients’ lives are significantly impaired. Impairment must occur in multiple settings to be classified as ADHD. [32] As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria.

In the USA these criteria are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified: ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months ADHD, Predominantly Hyperactive-Impulsive Type: if criterion 1B is met but criterion 1A is not met for the past six months. 113] The previously used term ADD expired with the most recent revision of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

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