UNIVERSIDAD ANÁHUAC MÉXICO
Campus Norte
FACULTAD DE PSICOLOGÍA
ADHD
Nombre: P. Janeth Guerrero Medrano
Materia: Psicofarmacología
Profesor: Héctor Romo
Semestre enero-mayo 2019
Huixquilucan, Estado de México, a 11 de abril de 2019.
A Review of the Pathophysiology, Etiology, and Treatment of Attention-Deficit Hyperactivity
Disorder (ADHD)
Pathophysiology
Attention-deficit hyperactivity disorder (ADHD) is among the most common neurobehavioral
problems afflicting children between 6 and 17 years of age. they may experience: impulsive
behaviour, slower rates of processing the information, low self-esteem, which leads to problems in
social relationships, tendency for substance abuse, and problems with law. About 60% to 80% of
the symptoms of ADHA persist into adulthood.
Etiology of ADHD
- Reduced volume or functionality of grey and white matter in the brain, leading to deficits in
cognitive processing, attention, motor planning, speed of processing responses, and other
behavioural issues.
- DA receptor density in several brain regions of ADHD patients is lower than normal.
- Disruption of a2 receptor function leads to impaired attention and impulse control and
hyperactivity.
- Reduced DA and/or NE function hypothesis in ADHD.
- Several studies pointed toward a hyperactive DA and/or NE system
- Males are 3 times more likely to have ADHD than females, and exhibit the predominantly
hyperactive or combined type, whereas females are more likely to exhibit the predominantly
inattentive subtype.
- We should make sure that there are no other underlying disorders that may potentially be
mislabelled as ADHD.
Treatment of ADHD
Treatment may consist of drug therapy, behavioural therapy or the combination. Early and effective
treatment has been reported to yield a better prognosis and fewer problems in adulthood. Drug
therapy was purported to be more effective than behavioural therapy. Some studies found that drug
therapy was superior to behavioural therapy in managing ADHD symptoms. Behavioural therapy
was useful, but the effect was not as robust as drug therapy. It may be useful for ADHD patients
with mild symptoms and minimal impairment to prefer behavioural therapy over drug therapy.
Drugs for treating ADHD include stimulants and non-stimulants,
Stimulants: The stimulants interact with and inhibit DAT-1 and nor- epinephrine transporter
(NET), thereby inhibiting the reup- take of DA and NE. Methylphenidate and amphetamines are
considered as equally efficacious for long-term treatment of ADHD. Amphetamines and
methylphenidate are ranked as 6th and 12th for substances known to cause physical harm. However,
stimulants do not seem to inhibit the NET and DAT-1 nucleus accumbens, when taken as
prescribed. Treatment ADHD with stimulants may decrease the risk of substance abuse.
Stimulant treatment has also been shown to decrease the likelihood for emergence of MDD, ODD,
and anxiety disorders65 and reduce aggression and antisocial behaviour in individuals with ADHD
Stimulants do not seem to enhance learning or improve academic performance in children or
occupational performance in adults diagnosed with ADHD. Stimulants have the capacity to
normalize attention in ADHD patients, but have been associated with initial reduced physical
growth, therefore, it is recommended to evaluate children on stimulants every 6 months for height
and weight.
Some of the side effects are gastrointestinal tract-related side effects, insomnia, and anxiety.
- Methylphenidate: it is much less likely to produce dependence and physical harm. DA
concentrations in the brain are increased by methylphenidate only when DA is being
released actively in the brain, such as during complex cognitive tasks
- Amphetamine salts: common side effects are similar to that of methylphenidate. It carries a
potential risk for abuse and dependence, however, the release and absorption of
amphetamine is slower with lisdexamfetamine.
Non-stimulants
The FDA approved nonstimulants for treating ADHD are atomoxetine (Strattera) and extended-
release α-2 agonists clonidine (Kapvay) and guanafacine (Intuniv).
Nonstimulants are believed to possess a less-robust effect than stimulants. Generally, take several
weeks to show their full effect.
- Atomoxetine (Strattera) is approved by the FDA for treating ADHD in children, adolescents,
and adults. It increases the availability of both NE and DA in the synapses of PFC. Requires
at least 4 to 6 weeks to show full effect, and it’s less likely to be abused than stimulants.
However, warnings regarding rare hepatotoxicity and suicidal ideation in children and
adolescents were issued by the FDA in 2005.
- a2 agonists (guanfacine and clonidine. These drugs may possess inferior efficacy as
compared with stimulants but may be as efficacious as behavioural therapy. Thus,
behavioural therapy is recommended before using these agents. They act on the presynaptic
and postsynaptic a2 receptors. Benefits observed after 4 weeks.
- Bupropion: inhibits the reuptake of both DA and NE but does not carry the potential risk of
abuse and dependence seen with stimulants, but it was been associated with seizures, so it
should not be used in patients with seizures or eating disorders.
- Tricyclic Antidepressants: have been the most widely used. No risk of abuse potential. Not
preferred nowadays because of a large number of cardiovascular, neurological, and
anticholinergic side effects and drug interactions. They have lesser efficacy than stimulants.
Treatment guidelines
Physicians have to rely on their clinical experience, the patient or their family’s preference,
presence of comorbid disorders, and any other medical conditions that may preclude the use of the
agents of choice. Periodic assessment to determine continued efficacy, safety, and need for
pharmacotherapy. A continuous monitoring not only ensures the continuous efficacy and
physical/mental well-being, but may also provide evidence for cessation of therapy.
References:
Sharma, A., Couture, J. 2014. A Review of the Pathophysiology, Etiology, and Treatment of
Attention-Deficit Hyperactivity Disorder (ADHD). Annals of Pharmacotherapy. Vol. 48, 209-225.
