Attention Deficit Hyperactivity Disorder (ADHD) involves problems with inattention, hyperactivity, and impulsivity and can occur in genetically predisposed people who are affected by environmental, neurobiological, and neuropsychological contributing factors. Some symptoms of ADHD are due to weak prefrontal cortical circuits that do not regulate attention and behavior adequately. Psychostimulants are the first line treatment for ADHD. If a patient can not tolerate or does not respond to this type of medication, alternatives can be norepinephrine agonists and antidepressants. Psychotropic medications mainly act on hyperactivity, impulsivity, and inattention and therefore psycho-educational and cognitive behavioral therapy are needed to address patient education and self-esteem, emotion management and organizational skills.
Attention deficit hyperactivity disorder (ADHD) involves a triad of problems with inattention, hyperactivity, and impulsivity (Surman, 2007a). It can occur in genetically predisposed people who are affected by environmental, neurobiological, and neuropsychological contributing factors (Simpson & Plosker, 2004). It usually appears in children before they reach seven years old (Faraone, 2007) and approximately 5 to 9 % of children in the US have this disorder (Young, 2002). Around 65% of children with ADHD do not outgrow it and therefore experience a chronic course of ADHD throughout their lifespan, which equates to approximately 4.4% or 9.4 million adults in the US (Surman, 2007a). Less than 11% of these adults ever attain treatment for their ADHD (Surman, 2007b). In addition, it is estimated that the ratio of males to females who have ADHD is somewhere between 3 to 10 males for every female (Marks, 2004). It is interesting to note that 50% of people referred to psychiatrists have ADHD (Barzman, Fieler, & Sallee, 2004).
Adults with severe cases of ADHD, left untreated, may never be able to live to their full potentials leaving behind what appears to be a train wreck of unfinished projects, destroyed relationships, and careers stopped mid-track due to temper tantrums, impulsive walkouts, and unfinished business (Steinhoff, 2007). Adults with ADHD have higher divorce rates, are involved in more vehicle accidents, have more encounters with the law, and are more likely to abuse alcohol or illicit drugs than adults without ADHD (Steinhoff). In addition, adults with ADHD tend to have lower incomes by $10,000 after controlling for educational and other relevant factors, higher number of past employers, and a higher incidence of unemployment (Young, 2007). The purpose of this paper is to first briefly examine the history and diagnosis of ADHD and afterwards to present current etiologies and therapies found effective in the treatment of adult ADHD.
History of ADHD
The first appearance of what seemed to be a description of ADHD was in 1902 by pediatrician Dr. George Still (a rather paradoxical name for someone observing hyperactive children) who described some children as lacking “volitional inhibition” and having an “abnormal defect of moral control” (Chiappa, 2003). Dr. Still hypothesized that these children’s behaviors were due to genetic factors or brain injury at birth (Chiappa). In 1955, researchers observing children with the same symptoms used the same explanation as Dr. Still and referred to it as “minimal brain damage” despite any neurological evidence (Chiappa). Ten years later, the disorder was renamed “hyperactive child syndrome” to describe the behavior rather than the presumed etiology. In 1968, the name was changed again and appeared for the first time in the Diagnostic Statistical Manual (DSM) as “hyperkinetic reaction of childhood” to reflect the psychoanalytic thinking of the time in which the disorder was presumed to be a reaction to adverse environmental stimuli such as abuse and neglect (Chiappa). In 1980, the DSM-III committee renamed the disorder “attention deficit disorder” in order to reflect the cognitive rather than behavioral issues inherent in this disorder (Chiappa).
ADHD was first conceptualized as a disorder only occurring in children (Chiappa, 2003). However, in 1972, researchers documented adults that did not outgrow the syndrome (Chiappa). In response, ADD residual type was added to the DSM-III to include these adults (Chiappa). In 1987, the new addition of the DSM-III-R reclassified the disorder as “attention deficit hyperactivity disorder” (Chiappa) (and this category remains today in the DSM-IV-TR). However, criteria used to diagnose children, such as “has difficulty playing quietly” were not relevant to adults, and therefore it was difficult to diagnose adults (Chiappa). The DSM-IV removed the modifier “residual type” and edited the symptom descriptions so that they became relevant for the diagnosis of adults (Chiappa).
Diagnosis of ADHD
The current DSM-IV-TR’s criteria for ADHD are that patients must experience six or more symptoms of inattention such as inability to attend to details, inability to sustain attention, inability to follow through on directions to completion and six or more hyperactivity-impulsive symptoms such as fidgeting or squirming, running, climbing, or talking excessively. These symptoms must persist for at least six months and be disruptive to one’s daily functioning. In addition, the symptoms need to be present before age seven, be present across settings, impair functioning, and are not a symptom of another disorder (DSM-IV-TR, APA, 2000). The DSM-IV-TR also specifies combined, inattentive, and hyperactive types, depending on whether one class (inattention versus hyperactivity) of symptoms is more predominant than the other, or whether both classes are experienced equally.
Brown (2007) notes that the DSM-IV-TR’s criteria for diagnosis were developed on data based on children and adolescents and that strictly adhering to these criteria only identifies adults with the most severe cases of ADHD. Brown argues that the critical issue for diagnosis of adults should be how impaired the adult is by these symptoms instead of the number of symptoms proposed by the DSM-IV-TR. Brown states that adults with ADHD tend to display six symptom clusters which usually respond together in treatment and are related executive cognitive functions that depend on or interact with each other. The six symptom clusters are problems with (a) organizing, prioritizing and initiating tasks, (b) focusing, sustaining and shifting attention, (c) regulating alertness, engaging in persistent effort such that they can not sit still, be quiet, or stay alert unless moving or speaking (d) emotional dysregulation such that they experience difficulties inhibiting frustration, anger, irritability, sadness and other emotions (e) working memory and recall and (f) self regulating action such that they have difficulties with hyperactive and impulsive behavior (Brown).
Overt signs of ADHD in children may be expressed differently in adults (Faraone, 2007). For example, hyperactive adults may feel restless, may be unable to sit for a long period of time, and may pace, shake their legs, tap pencils, pick their fingers, fidget, and talk excessively whereas children tend to run and climb excessively (Faraone). In addition, impulsive adults often make important decisions rashly without weighing options, often walk out of jobs without having another one in place, and end relationships without much forethought whereas children may suddenly hit or bite others (Young, 2007). Both children and adults with ADHD may blurt out answers or comments in the classroom or in discussion with peers, interrupt others, make impulsive comments, impulsively spend money, and have poor ability to inhibit emotional reactions (Faraone). However, as some children with ADHD age, the hyperactivity and impulsiveness can remit while the inability to pay attention remains (Dige & Wik, 2005).
It is important to note that people with ADHD are usually capable of maintaining concentration on tasks they find highly stimulating and interesting, but can not pay attention despite their efforts when tasks are not as stimulating (Brown, 2007). This problem leads some people to wrongly believe that ADHD is a matter of willpower, when actually etiologies that include genetic, structural and catecholamine explanations can account for this difficulty.
Consistent converging evidence from genetic, neurophysiological, and neurocognitive research points to a disorder of the brain in which executive functioning has gone awry. The problems with executive functioning start at the genetic level and involve prefrontal and frontal brain structures and key catecholamines.
Approximately 76% of ADHD can be attributed to genetics and 24% can be attributed to environmental factors (Faraone, 2007). Thus, both genes and environment interact to create this disorder (Faraone). Environmental factors than can contribute to the expression of ADHD are exposure to toxins during pregnancy, such as alcohol and nicotine, and obstetric complications (Faraone).
There are several genes that can make one susceptible to the expression of ADHD (Faraone, 2007). Specific genes that increase susceptibility are ones that encode for the D4 and D5 (dopamine) receptors as well as dopamine and norepinephrine transporter genes (Faraone).
In addition, synaptosomal protein of 25 kilodaltons, referred to as the SNAP-25 gene, has been shown to have a large influence on hyperactivity through research using coloboma mice (Jones, Williams, & Hess, 2001). These mice display symptoms of ADHD in that they are hyperactive and they do not stay with one activity for very long (Jones et al.). These mice are missing part of chromosome 22, the area in which SNAP-25 genes occur (Jones et al.). The SNAP-25 gene controls activity of neurotransmitters at the synapse in that it controls synaptic vesicle transmission and formation (Faraone, 2007): Dopamine is formed in little bubbles that are emitted into synapses (Faraone). Amphetamines enter the intracellular fluid and pop these bubbles thus releasing dopamine and facilitating the process of reverse transport through dopamine transporters (Faraone). When researchers injected these mice with functional SNAP-25 genes, the hyperactivity remits (Jones et al.). However, humans missing SNAP-25 genes can not attain similar treatment (Faraone). Other important factors involved in the expression of ADHD are brain structures in the prefrontal and frontal cortex.
There is no discord in the literature with regard to the prefrontal and frontal lobes as the main areas that are affected by ADHD. These lobes are believed to be the location in which functions such as motivation, self-reflection, self-regulation, and inhibition of impulses are situated (Barzman et al. 2004). The neuropathways that connect subcortical structures to the frontal lobes and the cerebellum are involved in ADHD (Faraone, 2007).
Using neuropsychological testing, Dige and Wik (2005) suggested ADHD symptoms were associated with reduced ability of the dorsolateral prefrontal cortex and subcortical regions related to this area. They found that people with ADHD (as compared to people without it) had slower processing speeds, less conceptual flexibility, substantially lower short term memory capacities, as well as less ability to manage tasks, plan, monitor working memory, encode information to long term memory, and remember after a delay.
In a meta-analysis of neuropsychological test results comparing people with ADHD to people without, Woods, Lovejoy, and Ball (2002) found a “wealth of empirical data” (p.13) that associated the cognitive symptoms of ADHD (attention and executive functioning) to frontal-subcortical systems. More specifically, some common differences found on neuropsychological measures were that people with ADHD had poor ability to estimate time, slower reaction times, protracted attentional blink suggesting difficulty shifting attention, poorer performance on selective visual attention, poorer memory, difficulty with inhibition, poorer nonverbal working memory, more difficulty controlling interference, poorer response organization, difficulty planning, poorer delayed free recall, poorer verbal fluency, poorer working memory, lower arithmetic subtest scores, poorer long delay free recall, longer visual orienting times, poorer logical memory, lower scores on measures of mental flexibility, lower scores on psychomotor speed, and poorer pattern recall (Woods et al.)
There are also subtle differences between males’ and females’ brains and substantially more males than females are diagnosed with ADHD (Young, 2007). Possible explanations for this difference could be simply that males tend to be more hyperactive and act out more than girls and therefore boys are more likely to be noticed by parents and teachers and more likely to be referred to a physician than girls. However, it has also been suggested that the male brain overproduces and then kills striatal dopamine receptors whereas the female brain does not engage in the process (Anderson & Teicher, 2000). Many of these brain structures depend on transportation and release of dopamine and other neurotransmitters.
It was originally thought that ADHD was a function of hyperarousal and that medications with sedating effects could ameliorate the symptoms (Arnsten, 2007). However, as technology advanced and brain imaging became possible, it became apparent that ADHD could be better explained in terms of weak prefrontal cortical circuits that do not regulate attention and behavior properly (Arnsten). The main catecholamines thought to be responsible for regulating attention and behavior are dopamine and norepinephrine. These neurotransmitters work together to modulate norepinephrine in posterior locations thought to be responsible for changing focus to new stimuli, attending to important stimulus characteristics, and ending focus on previous stimuli (Barzman et al., 2004). Executive functions mediated by both neurotransmitters in anterior locations are thought to be responsible for analyzing data and preparing for a response (Barzman et al.).
Krause, La Fougere, Krause, Ackenheil, and Dresel (2005) found that people with ADHD had low availability of striatal dopamine transporter. Using SPECT photography, they studied 18 people with ADHD who were not initially on medication. They took before and after medication images. Participants were titrated in a 10 week period to 60 mgs of methylphenidate. They found the highest concentration of the medication in the basal ganglia. They also found that six people did not response to methylphenidate and 12 did respond. Five of the six nonresponders had lower than normal striatal dopamine transporter availability whereas all the responders had elevated striatal dopamine transporter availability suggesting that people with low availability of this transporter will not likely respond to methylphenidate.
One theory suggests that norepinephrine is not sufficiently modulated in the ADHD brain and fails to ready the posterior attention system for external stimuli while deficient dopamine levels cause problems with attention (Barzman et al., 2004). This theory was formulated on the basis of medications that increase synaptic concentrations of norepinephrine and relieve symptoms of ADHD (Barzman et al.).
Alpha-2 agonists, such as clonidine and guanfacine, stimulate post-synaptic alpha-2A receptors located on dendritic spines of prefrontal pyramidal cells which serves to enhance connections in the prefrontal lobe networks and then enhances modulation of attention and behavior (Arnsten, 2007). Most of the alpha-2 receptors are postsynaptic norepinephrine terminals (Arnsten). When norepinephrine terminals and associated presynaptic alpha-2 receptors are destroyed, the brain increases the amount of alpha-2 receptors (Arnsten). Therefore, psychopharmacological treatment that addresses dopamine and norepinephrine activity is usually effective in controlling the symptoms of ADHD.
As ADHD is a disorder involving neurochemical functioning of specific neural networks, multimodal treatment involving medications and psychotherapy is usually beneficial in alleviating most symptoms. It is also important to note that conditions that need close monitoring when taking medications for ADHD are untreated hypertension, structural heart defect, heart arrhythmia, active substance abuse disorder, history of a psychotic or bipolar disorder, glaucoma, and seizure disorders (Surman, 2007b).
Medications effective in the treatment of adult ADHD include stimulants, norepinephrine agonists and antidepressants. It is interesting to note that approximately twenty drugs have FDA approval for ADHD in children, but only a few have been approved for use with adults, however, most drugs that are safe and effective for children are usually no different for adults (Young, 2007).
Psychostimulants are the first line treatment for ADHD (Barzman et al., 2004; Faraone, 2007; Young, 2007). For example, in a meta-analysis of 15 studies, including approximately 4500 adults with ADHD, Faraone et al. (2006) found a larger effect size for stimulants (both short and long acting) than nonstimulant medications. Psychostimulants such as methylphenidate and amphetamine affect dopamine transporters (Faraone, 2007). Earlier research using positron emission tomography (PET) suggested that methylphenidate substantially increased dopamine levels at the extracellular level by preventing dopamine transporter thus increasing dopamine concentration (Barzman et al, 2004). However, later research suggested that the imaging technology was not able to detect the delicate norepinephrine actions in the prefrontal cortex which exert a greater effect on executive functions than dopamine (Arnsten, 2007). Thus, stimulants facilitate endogenous stimulation of the catecholamines, mostly norepinephrine and dopamine, in the prefrontal cortex more so than subcortical structures which enhance the brain’s ability to pay attention to specific stimuli and decrease distractibility by amplifying weak signals thus decreasing background firing rates and increasing reception of target neurons (Arnsten.). In addition to stimulants allowing the brain to pay attention and decrease distractibility, Boonstra, Kooij, Oosterlaan, Sergeant, and Buitelaar (2005) found stimulants (such as methylphenidate) decrease perseveration so that attention can be switched to novel tasks.
It also appears that methylphenidate increases dopamine which affects motivation and reward centers in the ADHD brain which promotes interest in a task and therefore improves performance (Barzman et al., 2004). FMRi’s on people with and without ADHD who were given methylphenidate have not shown significant differences in specific circuits or sites. It is hypothesized that this nondifference means that only the magnitude and not the route in the ADHD brain is different (Barzman et al.).
Dose of methylphenidate is also important. In a meta-analysis of 19 studies on methylphenidate dose-response relationship, a dose of 0.6mg/kg/d resulted in a less than 50% response rate, whereas doses over 0.6mg/kg/d showed higher response rates (Wilens & Rostain, 2007). For example, Biederman et al. (2006) achieved a 66% response rate with a dose of 1.3mg/kg daily, although this dose was accompanied by a significant rise in both systolic and diastolic blood pressures as well as heart rates. Methylphenidate can be taken transdermally using a patch that produces steady delivery throughout the day but has only been approved in the treatment of children with ADHD (Young, 2007). Osmotic release methylphenidate has demonstrated effectiveness with adults. In a study of 394 adults, effect sizes were .38 for doses of 18 mgs, .43 for 36 mgs, and .62 for 72 mg doses (Wise, 2007). Possible side effects of methylphenidate are insomnia, loss of appetite, weight loss, gastrointestinal distress, irritability, increase in blood pressure and heart rate, and blunted mood (Goodman et al.; Steinhoff, 2007).
Some patients take one dose of a long acting stimulant and find that they need a booster late in the afternoon (Surman, 2007c). Surman suggests prescribing a short acting version of the same stimulant so that people can make it through late afternoon business meetings, classes or other attention demanding activities.
It appears that patients do not develop biological tolerance to methylphenidate (Steinhoff, 2007). Some patients report symptoms that appear to be tolerance after long term use; however physicians question whether people who have been on methylphenidate for a long time start to have expanded expectations of the drug’s abilities (Steinhoff). Weiss & Bailey (2003) suggest that if methylphenidate is taken as prescribed by a person without a substance abuse problem, it is unlikely that addiction will occur.
If a patient does not find methylphenidate effective or can not tolerate the side effects, amphetamines, such as dextroamphetamine or levoamphetamine in mixed salts, can be tried (Bailey & Weiss, 2003). Mixed amphetamine salts are available as a triple release system (one release after ingestion, one release four hours and one eight hours after ingestion) (Brown, 2007). Approximately 66% of adults with ADHD in Wilens, Findling, and McGough’s (2007) study taking mixed amphetamine salts experienced improved executive functioning, although 30% of the research participants suffered from insomnia that abated after time. Young, Wise and Surman (2007) found that the most effective dose was 50 mg, as compared to 25 and 75 mgs. Research participants from all three groups (25, 50, and 75 mg doses) showed improvement over placebo in one week (Young et al.). Young et al. found that the incidence of side effects, combined over the three dose levels, were that 42% experienced insomnia, 31% had decreased appetite, 26% had dry mouth and 21.5% developed headaches which abated over time.
In a study of 248 adults, Weisler (2006) found that all three groups who were given either a dose of 20, 40, or 60 mgs significantly reduced ADHD symptoms as rated by research participants on an ADHD symptom checklist. Psychostimulants work on the dopaminergic system whereas some nonstimulants work on the noradrenergic system (Young, 2007).
Alternatives to Stimulants
Approximately 30-40% of adults either can not tolerate the side effects of stimulants or do not respond well to them (Barzman et al, 2004; Wilens et al., 2007). For these patients, alternatives to stimulants such as norepinephrine agonists and antidepressants can be effective (Barzman et al.; Wilens et al.). One alternative is alpha-2A noradrenergic receptor agonists such as guanfacine and clonidine (Arnsten, 2007). Norepinephrine and dopamine regulate glutamate transmission (Wilens et al.). Glutamate is the main neurotransmitter in the brain (Wilens et al). The alpha-2 agonist receptor works at the post synapse receptor to enhance signaling (Wilens et al.). When norepinephrine is present, glutamate’s signaling is increased by closing a pore and preventing signal leakage (Wilens et al.). Enhancing glutaminergic transmission increases the brain’s ability to engage in executive functions, which occurs in the prefrontal areas (Wilens et al.). The alpha-2 adrenergic systems are sensitive to dose (Wilens et al.). Higher doses can prevent attention whereas lower doses can enhance it (Wilens et al.). Guanfacine is generally well tolerated at daily doses for adults at 1-4 mgs (Goodman et al. 2007). Common side effects are sleepiness and fatigue which tend to abate with time (Goodman et al).
A highly selective norepinephrine reuptake inhibitor is atomoxetine (Strattera), (Bailey & Weiss, 2003). This medication is useful for adults with ADHD who abuse alcohol as well as for adults with comorbid depression and or anxiety (Simpson & Plosker, 2004). Wilens et al. (2007) reported that heavy drinkers reduced their consumption by 30% while on atomoxetine over a three month study. This drug is not likely to be abused or diverted (Simpson & Plosker). Atomoxetine is usually well tolerated: side effects include possible dry mouth, insomnia, gastrointestinal problems, decreased appetite, constipation, dizziness, sweating, sexual problems, heart palpitations, and modest blood pressure and heart rate increases (Simpson & Plosker).
Atomoxetine can be effective for adults with ADHD, with a modest effect size of 0.4 (Steinhoff, 2007). In a study of 267 adults taking either 90 or 120 mgs daily of atomoxetine versus 248 taking placebo, 28.3% of the treated group and 18.1% of the placebo group reported symptom reduction (Simpson & Plosker, 2004). In addition, 42% of patients with emotional dysregulation problems reported reduced dysregulation problems while taking atomoxetine as compared to 19% of patients in the placebo group (Simpson & Plosker). The target dose is 80 mg per day with a maximum of 100 mg per day if needed (Simpson & Plosker)
Antidepressants have been used as a last resort and have been found effective for 30% to 40% of patients who did not respond to other medications (Barzman et al., 2004). For example, desipramine (Norpramin), a tricyclic antidepressant that blocks norepinephrine and serotonin uptake has been shown to be effective for some patients. Bupropion (Wellbutrin), that blocks dopamine reuptake has also shown efficacy with some ADHD patients (Bailey & Weiss, 2003).
One recent alternative to stimulants is Lisdexamfetamine (LDX), which is a new prodrug (Wilens et al., 2007). A prodrug is an inactive predecessor of a medication that once taken orally, is metabolized into an active form (Wilens et al.). The patient’s body becomes the delivery system in that the body’s metabolic processes release the drug so it can become active (Wilens et al.). Prodrugs exert their influence in more specific regions, are more reliably metabolized, and reduce toxicity (Wilens et al.). Prodrugs have the added advantage of not losing any potential because the prodrug is not metabolized into something else. As a result, prodrugs such as LDX, as compared to extended release amphetamine salts, have smoother rises, more consistent times to reach maximum plasma level, have less interpatient variability, and can control symptoms up to 12 hours on a single dose (Wilens et al.). Findling et al (2007) found that 95% of children who had taken LDX for one year experienced improvement of symptoms (46% of participants dropped out; 9% due to adverse effects, 4% due to lack of symptom relief). LDX has only been approved for the use of children, although studies of adults have shown it to be effective in adults with a history of substance abuse (Young, 2007).
In summary, psychostimulants are usually the first choice psychopharmacological treatment for adult patients with ADHD. If the patient can not tolerate or does not respond to this type of medication, other medications that can be tried are the norepinephrine agonists, and antidepressants. Psychotropic medications mainly act on the hyperactivity, impulsivity, and inattention part of the disorder and psycho-educational therapy is needed to address patient education, organizational and prioritization skills, self-esteem and other secondary disorders resulting from ADHD (Faraone, 2007).
Therapy that involves patient education regarding symptoms of ADHD, organizational skills, and management of emotion, behavior, social skills, stress, conflict and attention are usually beneficial for adults with ADHD (Wadsworth & Harper, 2007). Hessliner et al. (2002) developed a 13 session program that involved teaching the neurobiology of ADHD, mindfulness, controlling chaos, behavioral analysis, emotion management, depression, medications, impulse control, stress management, dependency, relationships, and self respect. They found significant improvements in a pilot study comparing eight people who completed therapy versus people on the wait list (Hesslinger et al.)
Furthermore, many adults with ADHD also have low self-esteem and depression after years of experiencing academic, vocational, and relationship failures that are partly due to symptoms of ADHD (Wadsworth & Harper, 2007). Many of these patients attribute their problems to moral or character defects which lead to guilt and depression (Kelley, English, Schwallie-Giddis, & Jones, 2007). Insight oriented and nondirective psychotherapies are usually not effective in assisting adults with ADHD (Wadsworth & Harper, 2007). However effective therapies include cognitive behavioral therapy (CBT) that addresses self-blame, guilt, and depression (Marks, 2004; Young, 2002).
Stevenson, Whitmont, Bornholdt, Livesay & Stevenson (2002) compared 22 people with ADHD on medication who completed a CBT group, 21 people without medication who completed a CBT group, and 21 people on a waiting list. Stevenson et al. found that people who completed the CBT group, regardless of whether they were taking medication, made statistically significant improvements on organizational skills, self esteem, and emotion management and that these improvements were evident at a one year follow up. Safren (2005) conducted a similar study comparing people who were provided with CBT and medication versus medication alone and found that 56% of patients improved with CBT and medication compared to 13% who had medication alone.
Neurofeedback has also been helpful as EEG waves of people with ADHD differ from those that do not have this disorder (Thompson & Thompson, 2005). Through displaying EEG biofeedback, patients learn to produce EEG waves that are present in states of calmness and alertness, thus controlling ADHD symptoms (Thompson & Thompson). However, this therapy would be a costly technique due to the need for specialized equipment.
In summary, alternatives or adjuncts to psychopharmacological treatments of ADHD mainly involves psychoeducational therapies that include information regarding the disorder, available medications, and organizational skills as well as CBT that addresses self-esteem, depression and emotion management. Neurofeedback also offers effective treatment although it is difficult to attain due to the necessity of specialized equipment.
ADHD can occur in genetically predisposed people who are affected by environmental, neurobiological and neuropsychological contributing factors (Simpson & Plosker, 2004). Consistent converging evidence from genetic, neurophysiological, and neurocognitive research points to a disorder of the brain in which executive functioning has gone awry (Faraone, 2007). This executive functioning involves genetic, environmental, and neurochemical influences that affect weak prefrontal cortical circuits that do not regulate attention and behavior adequately (Surman, 2007). Psychostimulants are the first line treatment for ADHD (Barzman et al., 2004; Faraone, 2007; Young, 2007). If a patient can not tolerate or does not respond to this type of medication, alternatives can be norepinephrine agonists and antidepressants (Wilens et al., 2007). Psychotropic medications mainly act on the hyperactivity, impulsivity, and inattention part of the disorder and therefore psycho-educational and cognitive behavioral therapy are needed to address patient education and self-esteem, emotion management and organizational skills (Faraone, 2007).
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