ADHD Medication is one of the most myth-ti-fied topics and lots of different people with their own agenda is polluting the debate – on purpose. We don’t care if you’re for or against ADHD medication, but we care about providing scientific and evidence-based knowledge, so here what we know so far …
ADHD as a diagnosable disorder can be traced back to 1775, and have undergone many revisions since then, until Dr. Russell A. Barkley, Ph.D. formulated the prevailing theory of ADHD in 1997 when he published his book ‘ADHD and the Nature of Self-control‘ which have become the de-facto standard for our scientific understanding of ADHD today.
ADHD medication has been used to treat symptoms of ADHD since 1937, and today there is 35 different medications that are FDA-approved. The most known to the general public is Ritalin which came on the market back in 1955 (Leahy, 2017).
Since then millions of people have used this and the other medications to reduce symptoms and thereby reducing impairments and improving quality of life Barkley Ed, R. A. (2014).
Today, it is estimated that 5.64% af the world’s population suffers from ADHD (Polanczyk et al., 2014), and of those most will require medicinal aid to cope with their mental disorder (Barkley, 1997).
Scientific studies on the causation of ADHD have repeatedly concluded that ADHD is a neurodevelopmental disorder which is genetic in its origin for the most part, although some are born with ADHD due to neurobiological contamination during pregnancy, in vitro (Franke et al., 2018)
People who suffer from Traumatic Brain Injury later in life, can also experience ADHD-like symptoms, which is often misinterpreted as Adult ADHD (Franke et al. 2018).
Since ADHD is a neurodevelopmental disorder, it cannot be acquired, it’s something you’re born with (Barkley, 1997) (Barkley Ed, R. A., 2014) (Franke et al. 2018).
People who get diagnosed late in life (30-40 years old) often realise that when their child is diagnosed and they see how well the treatment is working, that they too could get help (Barkley Ed, R. A., 2014).
We know that 25% of mothers and 30% of fathers, to a child with ADHD, have ADHD themselves, most likely undiagnosed and untreated. The same goes for the grand-parents which have the same risk as the parents (Barkley Ed, R. A., 2014).
That is why the rapid rise in drug usage for ADHD treatment can seem, to the untrained eye or wilfully ignorant person, to be growing at a rapid pace. There are perfectly reasonable explanations to this, and they include;
- Any disease that is relatively new in the diagnostic systems, will have a sharp increase in diagnoses, when clinicians and patients are being more aware of this novel condition. ADHD in its current form can be said to have been accepted since around 2000, which accounts for the rapid rise in medicated (children) patients in the past 15-20 years.
- Today in Europe, we are experiencing a rapid growth in medication again, this time it is due to the parents being diagnosed and medicated, as well as many grand-parents too are seeing the benefits of diagnosis and treatment and they too impact the growth in usage.
- In the US and New Zealand, pharmaceuticals are allowed to market directly to the customer for any product (‘ask you doctor …’) but this is not the case in the rest of the world, so when ‘Big Pharma Conspiracy Theorists’ claim that ADHD is something that Big Pharma have created to make money and point to the aggressive marketing af (ADHD) drugs in the US, they are missing the big picture, namely that the rest of the world actually have strict regulation on this and misuse, corruption and manipulating markets, are not as easy, as they think, based on their US understanding and expectations.
- All scientific evidence (more than 32,000 studies on ADHD from every thinkable angle, have been peer-reviewed and published in journals, as well as been available for studying at PubMed.Gov (click link to get the realtime list of published studies. The consensus is that ADHD is real, its biological, not psychological in nature, and just like Diabetes needs Insulin from outside the body to treat the symptoms of a chronic defect in the anatomy, ADHD needs to be treated with medication from outside the body, to treat its symptoms of the chronic defect of the neurodevelopmental disorders.
- ADHD is often called ‘The Diabetes of the Brain’ referring to the comparable nature of the biological underpinnings for both, and ADHD medication should be just as accepted and used, as Insulin is. Sadly, this is not the case. Since ADHD medication for the most part, contains amphetamine, which is known I the broad public as an illegal substance, many people misunderstand how amphetamine works in the brain, when you have ADHD.
- A brain with ADHD does not develop the needed neuronal pathways in vitro, as normal, but is delayed with upwards of 30-40% compared to a child at the same age. This causes the Inhibitory Control to be delayed in its development and since the Motor Control develops before the Inhibitory Control. This reverse order of development, causes the Motor Control to be ‘unmanaged’ by the Inhibitory Control, which is what causes the hyperactive, impulsive, inattentive symptoms, as well as the mind wandering, the emotional dysregulation and the impairments on Executive Functions in the brain.
- Therefore a brain with ADHD needs to be provided with a substance that can help the neurons build neuronal pathways in order to cope with this logistical nightmare of behavior, created by the lack of Inhibitory Control. For this process, a neurotransmitter called Dopamine is needed to help the brain create new neurons and synapses, that can connect the unruly parts of the brain to the Central Executive within the Prefrontal Cortex in the newest part of the human brain. Dopamine is the most significant neurotransmitters used to regulate behavior, since it is the body’s reward to the brain, for helping it survive and flourish. When the Dopamine levels gets above normal levels, people will feel a ‘high’ and some become ‘euphoric’ as well. This does not happen in the ADHD brain, since the natural level of Dopamine is very low, compared to the normal level, and by administering amphetamine to the brain with ADHD, you are able to increase the production of Dopamine, which in turn helps the brain better manage its functions – without – creating a feeling of ‘high’ or ‘euphoria’ since the levels of Dopamine never reaches or exceeds the normal level in the healthy brain.
- That is why people who rigorously postulate that parents of children with ADHD ‘just drug their kids because they are too lazy to parent them’ really display their utter ignorance about what ADHD is, causes and how its treated, based on scientific evidence. Some also believe that ADHD is caused by ‘bad parenting’ or ‘too much sugar, tv, iPad etc.’, or ‘lack of proper diet’ really haven’t understood what ADHD is, causes and is treated … at all …
- Furthermore the Internet is flooded with misinformation, either due to religious convictions about psychiatry (Scientology’s CCHR), political or financial interests and people who believe that their special brand of ‘alternative medicine’ or ‘functional medicine’ is the answer to all things related to ADHD. Its Not …There are very good studies of the various treatments for ADHD, medicinal, psychosocial, dietary etc., and they have been compared in 1:1 analysis, which overwhelmingly provide evidence for medication as the far superior treatment, compared to diets, fish oils, neurofeedback, and behavior modification therapy.
- Finally, the scientific consensus on the optimal treatment of ADHD is;
Medication first to handle the biological symptoms, then psychosocial support based on the understanding of ADHD not being a disorder that impairs your ability to learn knowledge, it is a disorder that impairs your ability to use what you know, before the lack of Inhibitory Control have already lost to the Motor Control, in the battle for projecting the desired behavior. With medication 80-90% of symptoms of ADHD are treated instantly and effectively, and medication is very safe also for usage over long-term.
The rest of this article is based on an excellent article by Dr. Leahy, and goes through the historical aspect of the diagnosis, as well as a complete list of all available ADHD medication on the market (US) today.
THE HISTORY OF ADHD
Symptoms now attributed to ADHD were first described in 1775 by Melchior Adam Weikard, a German physician, in Der Philosophische Arzt (Barkley, Peters, & Weikard, 2012).
By the end of the 19th century, Dr. Alexander Crichton noted the disabling features of ADHD, including restlessness, attentional difficulties, problems in school, and early onset (Palmer & Finger, 2001).
By the turn of the 20th century, Sir George Still (1902) conducted the first study of 43 children who demonstrated problems with self- regulation and sustained attention contributing to the inability to learn. Still (1902) further discussed these symptoms as “an abnormal defect of moral control in children” (p. 1008).
By the 1960s, a task force was developed to better understand this constellation of symptoms — then referred to as minimal brain dysfunction — which established the three core symptoms now associated with modern day ADHD: inattention, impulsivity, and hyperactivity (Clements, 1966).
With the advent of the Diagnostic and Statistical Manual of Mental Disorders (DSM; American Psychiatric Association [APA], 1952), minimal brain dysfunction was noted with a constellation of symptoms similar to those used today, although the disorder was thought to have its etiology in damage to the brain from illness or traumatic injury.
The working diagnosis in the second edition of the DSM became hyperkinetic reaction of childhood/adolescence; the key factor was that the behaviors diminished by adolescence (APA, 1968).
When the third edition (DSM-III) was published in February 1980, the world was first introduced to the diagnosis of attention-deficit disorder with or without hyperactivity, with onset before age 7 and symptom duration >6 months (APA, 1980).
The next revision, the DSM-III-R (APA, 1987), changed the diagnosis to ADHD and noted that “the disorder is frequently not recognized until the child enters school” (p. 57).
The DSM- III-R (APA, 1987) also noted that this disorder may persist into adulthood and that abnormalities of the central nervous system may be predisposing factors; prevalence at the time was indicated to be approximately 3% of children in the United States.
The fourth edition (DSM-IV; APA, 1994) changed the diagnosis to ADHD with three subtypes: predominantly hyperactive, predominantly inattentive, and combined. The DSM-IV noted that most individuals experience symptoms into late adolescence and adulthood, the disorder was common among first-degree relatives, and the prevalence was up to 5% in school-age children (APA, 1994).
The text revision of the DSM-IV (APA, 2000), which remained in use until the current fifth edition (DSM-5; APA, 2013), offered no change to the diagnostic criteria. Today, clinicians must use diagnostic criteria set forth by the DSM-5 (APA, 2013).
This latest edition moved ADHD from “Disorders Usually First Evident in Infancy, Childhood or Adolescence” to “Neurodevelopmental Disorders,” with an updated symptom onset of before age 12, allowing clinicians to more easily diagnose adults as it requires fewer symptoms to achieve diagnosis (APA, 2013).
This change also allowed ADHD to be diagnosed as a comorbid condition with autism spectrum disorders for those who meet both sets of diagnostic criteria (APA, 2013).
ADHD is now considered a neurobehavioral disorder, affecting approximately 11% of school-age children (Visser et al., 2014), with approximately 75% persisting into adulthood (Brown, 2013).
ADHD is characterized by symptoms of inattention, impulsivity, and hyperactivity, which are developmentally inappropriate and interfere with the individual’s ability to function in home, academic, occupational, and social settings.
Children with ADHD are at high risk for academic failure or delays, peer and family conflicts, risk-taking behaviors, substance abuse, motor vehicle accidents, and driving violations (Children and Adults with Attention-Deficit/Hyperactivity Disorder [CHADD], 2017a).
Although family conflicts do not directly cause ADHD, they can change the way in which ADHD manifests and may result in additional psychiatric issues, such as antisocial and criminal behaviors (Langley et al., 2010).
THE BIOLOGICAL AND NEUROCHEMICAL BASIS FOR ADHD
In addition to the external (i.e., social) and environmental (i.e., clinical) symptom presentations leading to a diagnosis of ADHD, there are also internal or biological bases, which are often more difficult to detect.
Such biological factors were compiled in a 2013 meta-analysis of the evidence-based genes associated with ADHD (Thapar, Cooper, Eyre, & Langley, 2013).
Collingwood (2016) also compiled evidence of genes related to ADHD.
Table 1: Genes related to ADHD.
Although genetics is only one component of the diagnostic conundrum, a meta-analysis of 1,800 genetic studies determined heritability of ADHD to be between 75% and 91%, and that multiple genes, as opposed to a single gene, were a likely factor (Zhang et al., 2012).
As nurses, we examine external and internal factors—the biopsychosocial factors—when evaluating an individual for potential diagnosis and treatment.
Thus, it is important to understand the entire context of how patients manifest their symptoms and explore the biological and genetic factors associated with a disorder, especially if pharmacotherapy is a potential treatment option.
The mechanism of action or neurochemistry of pharmacotherapeutic agents for the treatment of ADHD involves an understanding of the neuroscientific basis of the disorder.
It has long been believed that the neurochemicals serotonin, dopamine, and norepinephrine are responsible for most symptoms attributed to psychiatric illness, and the neurochemistry of ADHD is no exception.
The prefrontal cortex (PFC) or executive functioning portion of the brain is responsible for planning, organizing, reasoning, and control of impulses. Reduced levels of dopamine in the PFC impact memory and reinforcement, contributing to the symptoms of inattention and difficulty in memory formation (Conley et al., 2015).
Inefficiency in the transport of norepinephrine in the PFC leads to impulsivity, inattention, and hyperactive behaviors (Conley et al., 2015).
A decreased number of serotonin receptors, which aid in controlling impulses and improving the ability to think before acting, also leads to symptoms of hyperactivity and impulsivity seen in individuals with ADHD (Conley et al., 2015).
As a class, psychostimulant medications act by blocking the transport of dopamine and norepinephrine, leading to increased concentrations in the synaptic cleft, which in turn leads to increased neurotransmission of these neurochemicals and, ultimately, the improvement of ADHD symptoms (Stahl, 2013).
THE EVOLUTION OF PHARMACOTHERAPY FOR ADHD
Just as diagnostic criteria for ADHD have changed over time, so have pharmacological treatments.
Most psychostimulant medications used in the treatment of ADHD increase dopamine and norepinephrine in the PFC.
Although these drugs have existed for >80 years in the United States,their use did not become mainstream until the mid to late 1980s, when the diagnosis of ADHD was first published in the DSM-III and DSM-III-R.
A Romanian chemist first synthesized the amphetamine compound in 1887, but it took until 1929 for a California biochemist to discover its physiological and psychoactive effects while seeking a cure for asthma (Hicks, 2012).
The first psychostimulant/amphetamine tablet, Benzedrine® (racemic amphetamine), was introduced to the market in 1937 for the treatment of narcolepsy, postencephalitic Parkinsonism, and minor depression (American Medical Association Council on Pharmacy & Chemistry, 1937).
The following year, Dr. Charles Bradley, a psychiatrist treating children with behavioral disorders in a therapeutic home setting, serendipitously discovered that when Benzedrine was given to children to alleviate headaches resulting from testing involving pneumo encephalograms, their behaviors, school performance, and social and emotional reactions all improved (Strohl, 2011).
Bradley’s studies continued and ultimately shaped the pharmacological treatment of ADHD, albeit >25 years later (Strohl, 2011).
In 1943, Desoxyn® (methamphetamine) was introduced, but was not indicated for treatment of ADHD until decades later (Centers for Disease Control & Prevention [CDC], 2017).
Ritalin® (methylphenidate), arguably the “game changer” for the treatment of ADHD, was first synthesized in 1944 and first approved in 1955 for the treatment of chronic fatigue, narcolepsy, and depression in adults and geriatric patients (Center for Substance Abuse Research, 2013).
By 1963, the effectiveness of Ritalin as a treatment for emotionally disturbed children was being researched and published by C. Keith Conners, who went on to develop the many times revised and widely used Conners Comprehensive Behavior Rating Scales for parents and teachers in 1969 (Iannelli, 2017).
By 1975, the American Academy of Pediatrics’ Council on Child Health published their first official statement, “Medication for Hyperkinetic Children,” regarding use of psychostimulant drugs in children (Kugel et al., 1975).
Although amphetamine and mixed amphetamine drugs were discovered and synthesized since the late 19th century, Ritalin remained relatively unchallenged in the pharmaceutical marketplace until the mid-1970s when Cylert® (pemoline), DextroStat®, and Dexedrine® (both dextroamphetamine agents) were introduced.
Ritalin remained the gold standard until Adderall® (mixed amphetamine/ dextroamphetamine salt agent) was introduced in 1996 (after approved to be marketed in 1960) (CDC, 2017).
From 1997-2006, the diagnosis and subsequent pharmacological treatment of ADHD began a rapid period of growth in the United States, with a quadrupling of sales of psychostimulant medications (Pal, 2008).
Various new delivery systems for psychostimulant medications have been developed, some providing longer lasting beneficial effects on the symptoms of ADHD than others.
Despite being labeled as sustained release, many of the longer-acting psychostimulant agents did not provide coverage long enough to abate symptoms for an entire school day.
In 2000, when Concerta® (methylphenidate-OROS™) received marketing and sales approval from the U.S. Food and Drug Administration (FDA) (CDC, 2017), the pharmacological treatment of ADHD was again revolutionized.
Concerta became the first ADHD medication whose effects and abatement of ADHD symptoms lasted throughout the day on a single morning dose.
This new delivery system technology helped increase adherence and decrease visits to the nurse for a late morning or lunchtime dose of medication, which also reduced stigma associated with being a child medicated for ADHD (Coghill, 2002).
Since Concerta was introduced, many new delivery system technologies have been developed to offer personalized psychopharmacotherapy to individuals with ADHD. Although no new compounds or active ingredients have been synthesized over the past 17 years, methylphenidate, amphetamine agents, and mixed amphetamine salts have been produced in tablets, capsules, liquid, oral solutions, chewable tablets, transdermal patches, and orally disintegrating extended release tablets.
Table 2 shows the active ingredients and dosage forms of FDA-approved treatments for ADHD.
Table 2: Historical overview of the pharmaceutical agents used in the treatment of ADHD.
Psychostimulant drugs are not the only pharmacological agents approved by the FDA for the treatment of ADHD. Various non-stimulant medications with varied delivery systems, as well as a prescription medical food, have been the inception of
Strattera® (atomoxetine), a specific norepinephrine reuptake inhibitor (CDC, 2017), parents who were concerned about having their child prescribed and medicated with a controlled dangerous substance (CDS) now had alternatives.
All currently available psychostimulant drugs are classified as CDS Schedule II medications due to the high potential for abuse and dependency (FDA, 2017).
Strattera’s action of blocking the reuptake of norepinephrine allows for increased neurotransmission of norepinephrine and dopamine in the PFC (Bymaster et al., 2002), thus improving sustained attention and recall.
In 2009, Intuniv® (guanfacine) and Kapvay® (clonidine), both selective alpha-2 adrenergic antihypertensives in extended release delivery formulations, were introduced as non-stimulant alternatives (CDC, 2017). Intuniv and Kapvay improve the hyperactive and impulsive symptoms of ADHD by indirectly affecting dopamine by their initial action on norepinephrine in the PFC (CHADD, 2017b).
In addition to the three FDA-approved, non-stimulant medications available to treat ADHD, in 2013, Vayarin®, a prescription medical food, offered another alternative to those individuals wanting a more natural treatment (FDA, 2017).
Vayarin is said to reduce hyperactivity and improve attention by managing the lipid deficiency associated with ADHD through a unique compound of phosphatidylserine and omega-3 fatty acids. This medical food increases the bioavailability of lipid nutrients across the blood–brain barrier, which cannot occur simply through dietary modification (VAYA Pharma, 2016).
Since 1937, there have been 35 brand name drugs used in the treatment of ADHD. Only two — Biphetamine® (mixed amphetamine/ dextroamphetamine resin) and Cylert® (pemoline) — have been discontinued in the U.S. marketplace.
Although many of these drugs now have generic formulations available, pharmaceutical companies continue to manufacture brand name versions of the primary psychostimulant compounds (i.e., methylphenidate and various amphetamines), but with delivery systems offering unique features to allow for ease of portability and swallowing, improve adherence, and allow for patient preferences regarding taste and texture.
In addition, the varied delivery systems offer differing onset of immediate versus delayed action and overall duration of action depending on the formulation.
Prescribing clinicians can now offer a truly personalized treatment regimen to patients with ADHD.
ADHD has undergone many revisions and changes in its diagnostic label and pharmaceutical treatments over the past 80 years. Symptoms have been recognized for centuries, but have only been acknowledged as a viable disorder in children since 1980 and adults since 2013.
ADHD is known to have a complex etiology rooted in social and environmental spheres, as well as genetic and biological spheres. As holistic practitioners, nurses incorporate the biological, psychological, and social elements when evaluating patients. Nurses are in a prime role to identify and treat individuals across the lifespan who present with the symptoms of ADHD.
Just as the diagnostic label for ADHD has changed, so have the treatment options. Given the extensive role social and environmental factors play in the symptoms of ADHD, it is important to incorporate psychosocial therapies, behavior modification, and environmental manipulations in treatment plans for individuals with ADHD.
Psychopharmacology is simply another tool that can be incorporated in the treatment plan to address the biological and physiological underpinnings of this disorder, which impact functioning in the family, as well as in school/occupational and social settings.
As stigma remains regarding psychiatric disorders and specifically ADHD, the current historical overview and available pharmacological treatments can serve as a guide when clinicians are providing individuals and their loved ones with information regarding this highly treatable, old disorder.
American Medical Association Council on Pharmacy & Chemistry. (1937). Present status of benzedrine sulfate. Journal of the American Medical Association, 109, 2064-2069.
Blashfield, R. K., Keeley, J. W., Flanagan, E. H., & Miles, S. R. (2014). The cycle of classification: DSM-I through DSM-5. Annual review of clinical psychology, 10, 25-51.
Barkley, R.A., Peters, H., & Weikard, M.A. (2012). The earliest reference to ADHD in the medical literature? Melchior Adam Weikard’s description in 1775 of attention deficit (Mangel der Aufmerksamkeit, Attentio Volubilis). Journal of Attention Disorders, 16, 623- 630.
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121(1), 65–94.
Barkley Ed, R. A. (2014). Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment. Fourth Edition. Guilford Press. https://doi.org/10.1080/16506073.2015.1073786
Brown, T. (2013). A New Understanding of ADHD in Children and Adults. New York: Routledge,
Bymaster, F. P., Katner, J. S., Nelson, D. L., Hemrick-Luecke, S. K., Threlkeld, P. G., Heiligenstein, J. H., Morin, S. M., Gehlert, D. R., … Perry, K. W. (2002). Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: a potential mechanism for efficacy in attention deficit/hyperactivity disorder. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 27(5), 699-711.
Franke, B., Michelini, G., Asherson, P., Banaschewski, T., Bilbow, A., Buitelaar, J. K., … Reif, A. (2018). Live fast, die young? A review on the developmental trajectories of ADHD across the lifespan. European Neuropsychopharmacology, 28(10), 1059–1088. https://doi.org/10.1016/j.euroneuro.2018.08.001
Leahy L. G. (2017). Attention-Deficit/Hyperactivity Disorder: A Historical Review (1775 to Present). Journal of psychosocial nursing and mental health services, 55(9), 10-16.
Retrieved from http://www.cesar.umd.edu/cesar/drugs/ritalin.asp#4
Centers for Disease Control & Prevention. (2017). ADHD throughout the years. Retrieved from https://www.cdc.gov/ncbddd/adhd/ timeline.html
Children and Adults with Attention-Deficit/ Hyperactivity Disorder. (2017a). About ADHD.
Retrieved from http://www.help4adhd.org/Understanding-ADHD/About-ADHD.aspx
Children and Adults with Attention-Deficit/Hyperactivity Disorder. (2017b). Medication management.
Retrieved from http://www.chadd.org/Understanding-ADHD/For- Adults/Treatment/Medication-Management. aspx
Clements, S.D. (1966). Minimal brain dysfunction in children: Terminology and identification: Phase one of a three-phase project. Washington, DC: U.S. Department of Health, Education and Welfare.
Collingwood, J. (2016). The genetics of ADHD.
Retrieved from https://psychcentral.com/lib/the-genetics-of-adhd
Conley, M.B., Ellis, C.R., Hile, L.M., Mairena, C.J., Moseley, S.L., & Wert, T.J. (2015). Neurochemistry of attention-deficit/hyperactivity disorder (ADHD). Poster session presented at the Clemson University 10th Annual Focus on Creative Inquiry Forum, Clemson, SC.
Hicks, J. (2012). Fast times: The life, death and rebirth of amphetamine.
Retrieved from https://www.chemheritage.org/distillations/magazine/fast-times-the-life-death-and-rebirth-of-amphetamine?page=1
Iannelli, V. (2017). A history and medication timeline of ADHD.
Retrieved from https://www.verywell.com/adhd-history-of-adhd-2633127
Kugel, R.B., Scherz, R.G., Seidel, H.M., McMahon, J.L., Rinker, A., Garell, D.C.,… Poncher, J.R. (1975). Medication for hyperkinetic children. Pediatrics, 55, 560-561.
Langley, K., Fowler, T., Ford, T., Thapar, A.K., van den Bree, M., Harold, G.,…Thapar, A. (2010). Adolescent clinical outcomes for young people with attention-deficit hyperactivity disorder. British Journal of Psychiatry,
Leahy, L.G. (2017). From immediate release to long acting drug delivery systems: What do they mean and why do they matter? Journal of Psychosocial Nursing and Mental Health Services, 55(5), 19-23.
Pal, S. (2008). Patterns of diagnosed ADHD and LD, 1997-2006. U.S. Pharmacist. Advance online publication. Retrieved from
Palmer, E.D., & Finger, S. (2001). An early description of ADHD (inattentive subtype): Dr Alexander Crichton and ‘mental restlessness’ (1798). Child Psychology and Psychiatry Review, 6, 66-73.
Polanczyk, G. V., Willcutt, E. G., Salum, G. A., Kieling, C., & Rohde, L. A. (2014). ADHD prevalence estimates across three decades: an updated systematic review and meta-regression analysis. International Journal of Epidemiology, 43(2), 434–442.
Stahl, S.M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press.
Still, G.F. (1902). The Goulstonian lectures: On some abnormal psychical conditions in children. Lancet, 159, 1077-1082.
Strohl, M.P. (2011). Bradley’s benzedrine studies on children with behavioral disorders. Yale Journal of Biology and Medicine, 84, 27-33.
Thapar, A., Cooper, M., Eyre, O., & Langley, K. (2013). Practitioner review: What have we learnt about the causes of ADHD? Journal of Child Psychology and Psychiatry, 54, 3-16.
Food and Drug Administration. (2017). Drugs@FDA: FDA approved drug products.
Retrieved from https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm
VAYA Pharma. (2016). Vayarin: For health care professionals.
Retrieved from http://www.vayarinhcp.com
Visser, S.N., Danielson, M.L., Bitsko, R.H., Holbrook, J.R., Kogan, M.D., Ghandour, R.M.,… Blumberg, S.J. (2014). Trends in the parent- report of healthcare provider-diagnosis and medication treatment for ADHD disorder: United States, 2003-2011. Journal of the American Academy of Child & Adolescent Psychiatry, 53, 34-46.e2
Weizmann Institute of Science. (2017). Gene-Cards.
Retrieved from http://www.genecards.org
Zhang, L., Chang, S., Li, Z., Zhang, K., Du, Y., Ott, J., & Wang, J. (2012). ADHDgene: A genetic database for attention deficit hyperactivity disorder. Nucleic Acids Research, 40, D1003-D1009.
ABOUT THE AUTHOR
This article is written by Peter Vang from ADDspeaker.org, a non-profit grassroots organisation which works for the rights of persons suffering from Adult ADHD. ADDspeaker does not have any affiliation with or dependence of any religious, political, financial or pharmaceutical interests, and all work is done on a voluntary basis, without any financial or other gain.
ACKNOWLEDGEMENT: Built on and adapted from the article “Attention Deficit Hyperactivity Disorder: A Historical Review (1775 to Present)
by Laura G. Leahy, DrNP, APRN, FAANP
Leahy, L. G. (2017). Attention-Deficit/Hyperactivity Disorder: A Historical Review (1775 to Present). Journal of Psychosocial Nursing and Mental Health Services, 55(9), 10–16.
Dr. Leahy is Family Psychiatric Advanced Practice Nurse and Master Clinician in Psychopharmacology, APNSolutions, LLC, Sewell, New Jersey.
The author has disclosed no potential conflicts of interest, financial or otherwise.
Address correspondence to Laura G. Leahy, DrNP, APRN, FAANP, Family Psychiatric Advanced Practice Nurse and Master Clinician in Psychopharmacology, APNSolutions, LLC, 123 Egg Harbor Road, Suite 703, Sewell, NJ 08080, USA