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From the amygdala, dopamine exerts an effect on neurons within the hippocampus. Interactions in brain reward regions. When dopamine is released in the nucleus accumbens, it activates dopamine D 2 receptors, a key reward site. This release is also regulated by enkephalins acting through GABA.

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The supply of enkephalins is controlled by the amount of the neuropeptidases that destroy them. From the amygdala, dopamine stimulates the hippocampus and the CA and cluster cells stimulate dopamine D 2 receptors. It is to be noted that the putative glucose receptor in the hypothalamus is intricately involved and links the serotonergic system with opioid peptides leading to the ultimate release of dopamine at the nucleus accumbens.

In the brain reward cascade these interactions may be viewed as activities of subsystems of a larger system, taking place simultaneously or in sequence, merging in cascade fashion toward anxiety, anger, low self-esteem, or other unpleasant feelings, or toward craving of a substance that will reduce or eliminate the feelings eg, alcohol, carbohydrates, alcohol, and drugs Blum and Kozlowski b.

The notion of dopamine as the final common pathway for a number of diverse drugs of abuse is supported by the findings of Ortiz and associates Ortiz et al They demonstrated that chronic administration of cocaine, morphine, or alcohol resulted in several biochemical adaptations in the mesolimbic dopamine system.

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They suggested that these adaptations may underlie changes in the structural and functional properties of the neuronal pathway of this system related to substance abuse Ollat et al ; also see Imperato and Di Chiara Genetic anomalies, long-term continuing stress, or long-term abuse of substances can lead to a self-sustaining pattern of abnormal craving behavior in both animals and humans. Research on nonhuman animals has provided support for the cascade theory of reward and its genetic links.

Thus, Li and colleagues Russell et al ; Zhou et al ; McBride et al , ; Li et al developed strains of alcohol-preferring P and non-preferring NP rat lines. They found that the P rats have the following neurochemical profile: lower serotonin neurons in the hypothalamus; higher levels of enkephalin in the hypothalamus due to a lower release ; more GABA neurons in the nucleus accumbens; reduced dopamine supply at the nucleus accumbens; and reduced densities of dopamine D 2 receptors in the mesolimbic areas.

In terms of genetics, especially as related to ADHD, a number of genes have been associated, and these candidate genes are all involved in the reward cascade. Comings et al described a subset of at least 42 gene variants, which associate with ADHD and contribute to the overall variance.

Interestingly, these genes constitute the basis for the reward cascade including certain neurotransmitters but not limited to dopaminergic, serotonergic, enkephalinergic, catecholaminergic, cholinergic, GABAergic, androgen receptors, as well as other putative transmitters, hormones, and their receptors and enzymes both anabolic and catabolic. In recent years, a number of reviews of the neurochemical basis of ADHD have emphasized the involvement of multiple neurotransmitters and emphasized that one single genetic defect cannot explain all of the data. Polygenic inheritance is uniquely capable of answering the question of how to account for both the range of comorbid disorders in ADHD and their interaction, but it fails to provide us with a true model of subsets of genes and their contribution to the variance of the disorder in question.

Their results showed that these three genes were additive in their effect. Thus, individuals who had three out of three markers had the highest ADHD score; those with two of three had the next highest score; then one of three; and those with none of the three markers had the lowest ADHD score Comings et al In other words, the different associated behaviors are due to similar sets of genes in that certain psychiatric disorders have a number of genes in common.

This suggests a four-part cascade sequence leading to a reduction of net dopamine release in a key reward area. Additional support for this idea came when investigators found that by administering substances that increase the serotonin supply at the synapse, or by stimulating dopamine D 2 receptors directly, they could reduce craving for alcohol McBride et al Specifically, D 2 receptor agonists reduced alcohol intake in high alcohol preferring rats, whereas D 2 dopamine receptors antagonists increased alcohol drinking in these inbred animals Dyr et al In ADHD, the picture emerges of individuals suffering from overload, trying to adjust to a world that is too bright, too loud, too abrasive, and too rapidly changing for comfort.

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Early speculation about the causes of ADHD focused on such factors as marital disorder, poor parenting, brain damage, psychiatric illness, or alcoholism or drug abuse in the family. Associated behaviors included CD and anti-social personality.

Later these behaviors were shown to be linked hereditarily to substance use disorder SUD. Most recently, research has begun to show a significant association between these behavioral disorders, ADHD, and specific genetic anomalies. What is the cause or basis of ADHD?

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It is an impulse disorder with genetic components that results from imbalances of neurotransmitters. Its effects can be eased by treatment and counseling. The biological basis for this disorder has been established by a number of investigators Comings et al ; Biederman et al Their beta waves brain waves associated with concentration are low, and their theta waves associated with relaxation are high, suggesting a state of drowsiness and daydreaming. It is not surprising, therefore, that activities associated with beta waves, eg, watchful anticipation and problem solving, are difficult for individuals with ADHD to sustain.

They like activities that permit them to stay in a theta state with a minimum of outside stimulation Lubar It may be that people with ADHD are afflicted with a defective filtering system such that their brainstem reticular formation does not block out irrelevant stimuli.

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These people appear to be aware of every sound, every object, every touch, and they all merge in disorganized behaviors that are difficult to tolerate. Non-essential stimuli get the same attention as those essential to work or relating to other people. At a deeper level, ADHD is a problem of communication among brain cells, or neurons, possibly involving the neurotransmitters that carry inter-neural messages.

These brain messengers may be either in short supply for certain behaviors such as cravings probably due to inadequate serotonergic and or dopaminergic function or other attentional deficits, or they may be the result of too much norepinephrine rather than too little. If the messengers that inhibit incoming stimuli are deficient, too many signals get through and create confusion. At a still deeper level, the problem lies in the genes that lay down the blueprint for manufacturing neurotransmitters.

People with ADHD have at least one defective gene, the DRD 2 gene that makes it difficult for neurons to respond to dopamine, the neurotransmitter that is involved in feelings of pleasure and the regulation of attention. Support for the role of genetics in ADHD includes evidence showing that it runs in families.

As early as , James Morrison and Mark Stewart examined parents of 59 hyperactive children and 41 control children. In 21 of the families, at least 1 parent was alcoholic or had antisocial personality and other related behaviors. By contrast, only 4 of the control families were so affected. In a family study of parents and siblings of felons, there was an increased frequency of antisocial personality, alcoholism, and drug addiction in male relatives of hyperactive children Cantwet al This is 2—7 times the frequency found in non-ADHD children.

These siblings also were 5 times more likely to have major depression than control children Welner et al ; August and Stewart Interestingly, however, when ADD is considered without hyperactivity, the number of brothers and sisters affected was the same Cantwell The question can be asked, was the behavior learned? One answer to the question is to look at siblings and half-siblings, both raised in the same environment.

If ADHD is learned, the frequency should be the same for both. In actuality, half-siblings who have only half the genetic similarity show a significantly decreased frequency of ADHD Safer This finding was confirmed in other independent studies. Another approach is to look at the parents of ADHD children given up for adoption. If ADHD is a genetic disorder, the parents of children with the problem should show a higher frequency of ADHD, antisocial personality, or alcoholism than the adopting parents. In a study of ADHD children of ADHD parents who gave up their children at birth for adoption, it was found that the rate of antisocial personality, alcoholism, and ADHD was higher in the biological parents than in the adopting parents.

This was confirmed by Blum and associates To some extent, people with ADHD can learn to cope. They can avoid situations that generate stress; avoid crowds and noisy environments; give themselves plenty of time and avoid tight deadlines; and avoid rapid changes in their environment. The most destructive coping strategy is self-medication with alcohol or drugs.

Such substances give the illusion that they are making life easier and more pleasant, for the symptoms seem to disappear. But the addiction quickly takes over, and life becomes a nightmare Faraone et al Then, when they withdraw from alcohol or drugs, the ADHD problems return in full force. The inherent tragedy here is that the ADHD person may be genetically at risk of developing an addiction. In clinical settings, a number of rating scales have been utilized with mixed results for the diagnosis of ADHD.

Another alternative utilized in a clinical setting to assist in properly diagnosing ADHD is a continuous performance test called T. The latest version of this test is computerized, and it is designed to identify a minimum of four types of attention failures. The problem with relying on this parameter is that omission errors have been associated with a wide spectrum, including schizophrenia and petit mal seizure disorder, in which the attention failure is marked by neurological absences.

The second type is marked by commission abnormalities associated with impulsive behaviors, and it frequently is co-morbid with a cluster of anxiety disorders eg, obsessive compulsive behaviors, panic, and oppositional defiance. The third type is marked by abnormalities in reaction time. It is believed that this type is not specific for ADHD and is associated with slowing of response times as seen in classic psychomotor retardation, dysthymia, and major depression.

The fourth type is response variability either fast or slow. It is this fourth type that is most likely linked to dopaminergic deficiency. However, it is important to note that results of T. To test the relationship between response variability and dopaminergic deficiency, we embarked on a study that examined associations between dopamine D 2 receptor variants and T. We studied patients entering the PATH Medical Clinic, New York City, for a variety of medical complaints including neuropsychiatric, cardiovascular, and oncological problems.

Each patient was given the T. When all the T. Moreover, we found significant differences between the various scores inattention, impulsivity, response time, and variability and abnormal P latency Braverman et al In contrast, only variability response was significant for P amplitude. This site-specific association may be attributable to dopaminergic variants. It is well known that the DRD 2 gene A1 allele is associated with abnormalities in both the P latency and amplitude in well-screened alcoholics Noble et al Thus, we must caution the clinician in terms of utilizing only one diagnostic tool to diagnose ADHD.

We alternatively suggest that a number of tests including both Conners and T. Estimates of the frequency of the various types of ADHD, based on population surveys, have shown variable results.

A fairly common range is illustrated in Table 2. The advantage of population based samples, in contrast to clinic based samples, is that individuals in the community who have not sought medical attention are included in the sample. This is contrary to the notion that the ADHD is overdiagnosed and overtreated. In fact, the majority of symptomatic children are not treated.


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After Wolraich et al While many of these children can be handled by appropriate teaching methods and do not require treatment, these figures suggest that ADHD-I at least, is probably under diagnosed and under treated. This is a reflection of the fact that ADHD in girls tends to present as the inattentive type while boys are more likely to present as the hyperactive-impulsive or combined type.

Symptoms of hyperactivity and impulsivity in school are obvious and disruptive, whereas symptoms of inattention are more subtle and non-disruptive; consequently, boys tend to be diagnosed and treated more than girls. It has been known for many years that if an individual inherits enough genes to develop any given behavioral disorder, the risk of developing a second behavioral disorder is two to four times greater than for the general population. This is likely due to the fact that different behavioral disorders share some gene variants in common. Thus, the more a person exceeds the required threshold number of gene variants, the greater the likelihood of developing more than one behavioral problem, thus the term spectrum disorders.

Some of the most common coexisting or comorbid spectrum disorders seen in individuals with ADHD are ODD, CD, major depressive disorder, anxiety disorders, OCD, bipolar disorder, learning disorders, and substance abuse disorder including alcoholism and drug addiction. Having pointed out that much of the poor outcome in ADHD children is due to the comorbid presence of CD, we would still like to present the studies of a report of Howell and coworkers Howell et al The study compared the outcome of three groups of children instead of just ADHD children and controls.

They were then re-evaluated after they graduated from high school. The remarkable finding was that in virtually every aspect of their life the low ADHD group performed best, the normal individuals were intermediate and the ADHD group performed worst. This should not be taken to suggest that children with ADHD always underachieve. Again, we wish to emphasize there are many examples in which the restless, workaholic, always-have-to-be-doing-something, I-need-to-be-my-own-boss, characteristics of ADHD subjects result in very successful lives.

Thus, in the right combination, some of the symptoms we have been discussing in a negative light can be used to great advantage Comings et al It has been proposed that ADHD is a polygenic disorder due to the additive effect of genes affecting dopamine, norepinephrine, serotonin, GABA, and other neurotransmitters eg, see Comings et al In one recent study Brookes et al , 1, single-nucleotide polymorphisms SNPs spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, norepinephrine, and serotonin pathways, in addition to circadian rhythm genes, revealed interesting results.


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ADHD is not caused by poor parenting, family problems, poor teachers or schools, too much TV, food allergies or excess sugar.