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Attention Deficit Hyperactivity Disorder

HISTORY
Attention Deficit Hyperactivity Disorder was first described by William Still in 1902. It was later discovered that children who survived the viral encephalitis and meningitis outbreak in 1918 demonstrated symptoms of ADD. Over time, the terminology evolved from Still's original label of "morally defective" to "minimal brain damage" in the 1930's, and "minimal brain dysfunction" in the 1960's. Ultimately, it acquired the name we know today, ADHD. ADHD is a diagnosis applied to children and adults who consistently display certain characteristic behaviors over a period of time.

DIAGNOSIS

At present, ADHD is a diagnosis applied to children and adults who consistently display certain characteristic behaviors over a period of time. The most common behaviors fall into three categories: inattention, hyperactivity, and impulsivity.

  • Inattention
    Inattention refers to an individual’s inability to keep their mind on a task. Often the individual with ADHD may get bored with a task after only a few minutes. They may give effortless, automatic attention to activities and things they enjoy, but focusing deliberate, conscious attention on the organization and completion of a specific task is often difficult.
  • Hyperactivity
    Hyperactivity is the state or condition of being excessively or pathologically active. Hyperactive children have difficulty sitting still and sitting still through a lesson can be a very difficult task. Hyperactive children often squirm in their seats or roam around the room. Hyperactive teens and adults may feel intensely restless.
  • Impulsivity
    People who are overly impulsive seem unable to curb their immediate reactions or think before they act. As a result, they may blurt out inappropriate comments or run into the street without looking. Impulsivity can make it difficult for them to wait for things they want or to take their turn in games

Not everyone who is overly hyperactive, inattentive, or impulsive has an attention disorder. Since most people sometimes blurt out things they didn't mean to say, bounce from one task to another, or become disorganized and forgetful, how can specialists tell if the problem is ADHD?

To assess whether a person has ADHD, specialists must determine whether the behaviors are excessive, long-term, and pervasive. To make this assessment, the person's pattern of behavior is compared against a set of criteria and characteristics of the disorder.

According to the DSM-IV, there are three patterns of behavior that indicate ADHD. People with ADHD may show several signs of being consistently inattentive. They may have a pattern of being hyperactive and impulsive. Or they may show all three types of behavior.

According to the DSM, signs of inattention include:
  • becoming easily distracted by irrelevant sights and sounds
  • failing to pay attention to details and making careless mistakes
  • rarely following instructions carefully and completely
  • losing or forgetting things like toys, or pencils, books, and tools needed for a task
Some signs of hyperactivity and impulsivity are:
  • feeling restless, often fidgeting with hands or feet, or squirming;
  • running, climbing, or leaving a seat, in situations where sitting or quiet behavior is expected;
  • blurting out answers before hearing the whole question; and
  • having difficulty waiting in line or for a turn

Because everyone shows some of these behaviors at times, the DSM contains very specific guidelines for determining when they indicate ADHD. The behaviors must appear early in life, before age 7, and continue for at least 6 months. In children, they must be more frequent or severe than in others the same age. Above all, the behaviors must create a real handicap in at least two areas of a person's life, such as school, home, work, or social settings

CURRENT RESEARCH

Attention deficit hyperactivity disorder (ADHD) is a common psychiatric disorder affecting approximately 3 to 6% of school age children. ADHD is characterized by difficulties with attention, motor over-activity, and impulsivity that interfere with normal functioning in various settings. Currently researchers and physicians in the field regard ADHD as a neurological, biochemical disorder, no longer a behavioral disorder as was once believed. Numerous studies support the idea that ADHD is a developmental disorder that the individual is born with.

Generally, the primary motor deficit in these individuals (i.e., an inability to inhibit or delay motor responses) and other neuropsychological findings such as executive function deficits lead many researchers to speculate that striatal and prefrontal brain regions and related dopamine dysregulation may be involved.

In a recent comprehensive, combined cross-sectional and longitudinal structural imaging study of 152 ADHD adolescents and 139 age-matched controls, total brain volume reductions were confirmed. Regional frontal, parietal, temporal and occipital volume measures were all reduced in the ADHD patients without any regional distinctions. The anatomical effects were similar in ADHD patients with and without any previous drug treatment.

Functional imaging studies of ADHD patients have also indicated frontal dysfunction. Positron emission tomography (PET) with (18F)-fluoro-2-deoxy-D-glucose (FDG) has been used to show decreased frontal lobe metabolism in adults with during an auditory attention task. Functional MRI studies have shown hypoactivity of the anterior cingulate in adults with ADHD and hyperactivity of frontal regions in children with ADHD during

RESEARCH AT LONI
Subjects
In a recent study, twenty-seven ADHD subjects were selected from among a larger group studied previously because they met DSM-IV criteria for ADHD, they had no secondary diagnoses of obsessive compulsive disorder or Tourette Syndrome, and they had adequate brain imaging data for the purposes of these analyses. Subjects were excluded if they had any movement disorder or neurological illness, past seizures or history of head trauma with loss of consciousness, ongoing substance abuse or previous substance dependence, an IQ below 75, or a major psychiatric disorder predating an ADHD diagnosis.

Eleven girls and 16 boys with ADHD, and 46 normal controls were studied. The children ranged between the ages of 8 and 18. Subjects were excluded from participation if they had a history of concussion, substance abuse, or seizure disorder. Further, subjects were thoroughly screened for neurological impairments, psychiatric illness, history of learning disability, or developmental delay using a structured diagnostic interview either administered or reviewed by a board-certified child and adult psychiatrist (BSP). IQ measures did not differ significantly between the control and ADHD subjects.
 
Image Protocol

All subjects were scanned with a single 1.5 Tesla superconducting magnet. The MRI protocol collected was a whole-brain gradient-echo (SPGR) T1-weighted series collected in the sagittal plane.

 
Results

In this study, for the first time, we were able to map brain growth and gray matter density abnormalities in the cerebral cortex in boys and girls with ADHD. As predicted, significant dysmorphology was observed in the frontal cortex in the ADHD group. Specifically, reduced brain growth or brain shape abnormalities were observed in the more ventral aspects of the frontal lobes primarily in Brodmann’s areas 44, 45, 46, and inferior regions of area 6. Unpredicted but significant reduced brain growth was also observed bilaterally in the temporal lobes, primarily in the more anterior regions in Brodmann’s areas 38, 21 and 20. Gray matter density abnormality was shown in the temporal lobes bilaterally where the ADHD subjects had a 15 to 30% increase in segmented gray matter. Gray matter density in the inferior parietal lobes was also increased. While unpredicted in these regions, the gray matter differences in posterior temporal and inferior parietal lobes appear robust, and survive correction for multiple comparisons in the permutation analyses.

The relevance of more inferior dorsolateral cortex being reduced in size should not be lost in this study of ADHD. The mid-dorsolateral prefrontal cortex (i.e., Brodmann’s area 45) has been compellingly argued to subserve executive processes for the monitoring of information within working memory. Strong arguments have been made for links between working memory and response inhibition in Barkley’s theory of executive dysfunction in ADHD. Strong connections between the mid-dorsolateral prefrontal cortex and superior temporal gyrus have also been reported, providing support for our temporal lobe findings as well. Functional MRI studies have shown greater power of functional response in ADHD than control subjects in the medioinferior frontal lobe (i.e., area 45 9/45) during a response inhibition task. Thus, there is mounting evidence that the mid-inferolateral dorsal frontal cortices are affected in ADHD.

Gray matter density abnormalities in posterior temporal and inferior parietal lobes are actually the result of increased gray matter in the ADHD patients relative to controls. The increase in gray matter in these regions could result from reduced synaptic pruning that normally occurs as a part of human brain maturation. It is also plausible that a lack of normal myelination has occurred in this region. While we measured “gray matter density” at the cortical surface, arguably a reduction of white matter in the same region could result in an apparent abundance of gray matter.

The statistical maps for brain growth and gray matter density reveal suggestive differences between male and female ADHD subjects where the females appear to have greater brain growth abnormalities than the males, and the males appear to have greater gray matter density abnormalities than the females. However, the patterns of brain growth reduction and gray matter density increase are similar in both groups and statistical maps of group by gender interactions did not appear significant.

 
 
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