Introduction To The History Of ADHD

Welcome to the History of ADHD Timeline. While the history of ADHD is not the most exciting subject, it is necessary to answer the question: “Why do some folks say ADHD is not a real condition?” To answer this question, we must go back to the beginning, when the condition we know as ADHD was first observed, noted, and treated.

As you read through the History of ADHD, you will find many reference notations. If you wish to read the entire study, following this history is the complete reference. To be forewarned, some of these studies are hundreds of pages long!

 The History Of ADHD (1798-1944)

ADHD has undergone more iterations, evolutions, and convoluted twists and turns than any other condition afflicting humans (Stein, 2013). First described as a disturbance of brain nerves in 1798 by Baumeister and Henderson, ADHD has undergone a lengthy evolution of descriptions and diagnostic criteria. The name for the condition has changed no less than a half dozen times, as have descriptions and treatment options according to mental health professionals during the past two hundred plus years. According to Orendorff in 2009, this historical meandering of ADHD’s diagnostic history is perhaps what leads us to the present-day question: “Does ADHD exist?

The hypothesis of two prominent causes for ADHD was presented in 1902 by Tredgold; Brain Cell Metabolism and Defects in Moral Control. The encephalitis pandemic of 1917-1918 (Encephalitis is inflammation of the brain) resulted in several studies on ADHD, including Tredgold’s analysis on Neurological Orientation.  Tredgold postulated that rather than the trilogy of impaired attention, hyperactivity, and poor impulse control, the cause for the condition was Social Moral Decay. Tredgold also hypothesized that impaired concentration was associated with physiological components resulting from disease or injury to further muddy the water. Interestingly, Baumeister and Henderson discovered that Tredgold’s and Crichton’s studies, separated by roughly 178 years, arrived at the same conclusion: ADHD had a neurobiological origin.

Further support for Tredgold’s hypothesis came from studies from the post-Encephalitis Pandemic of 1917-1918 when children who survived the Encephalitis outbreak exhibited the same symptoms. This cluster of symptoms—poor impulse control, hyperactivity, and inattention became known as the Holy Trinity of ADHD. Tredgold’s study led to much interest within the medical and scientific communities, as additional studies were published that investigated links between ADHD and birth trauma, childhood measles, and head trauma.

Studies following the Encephalitic Pandemic of the 1920s pointed to encephalitis as the cause of ADD, with three more labels connecting Encephalitis with ADD (Attention Deficit Disorder): Basal Ganglia Damage in 1929, Brain Stem Damage in 1931, and Brain-Stem Lesions in 1934.

In 1937,  performed Spinal Taps on children with the condition to research abnormalities in spinal fluid, which resulted in severe headaches in the studied children. To alleviate the intense headaches, Dr. Charles Bradley administered stimulants. To Dr. Charles Bradley’s surprise, he began receiving reports over the following several days suggesting the general disposition of the ADHD group had improved significantly, and they were behaving like normal children in the class. During this same period, ADHD saw its first implication in girls, described by teachers and parents as having schizoid episodes. According to Schachar, Rtrrrer, & Smith in 1981, a follow-up study involving the administration of stimulant medication to alleviate symptoms of ADHD saw similar results from the boys. A hundred years would pass before the connection between ADHD and TBIs (Traumatic Brain Injuries) would be made as a secondary cause of ADHD, aside from genetic heritage.

In 2001, Palmer & Finger discovered laboratory studies in the 1940s involving animals with frontal lobe lesions that strengthened the relationship between ADHD and the pathological brain changes resulting from Restless Brain Syndrome. Restless Brain Syndrome studies continued to drive research well into the 1950s and 1960s with two new labels given to the condition: Minimal Brain Damage and Minimal Brain Dysfunction, both with the acronym MBD.

A period of concentrated studies resulted from synthesizing and releasing the stimulant medication Ritalin in 1944.  This period of focused research would continue to ramp up exponentially between 1944 and 2014. A compilation of studies performed by Baumeister and Henderson discovered that between 1957 and the early 1980s, ADD was linked to Seizures, Deficient Cortical Inhibition of Subcortical Structures, and lower Intelligence Quotient (IQ) levels.

The History Of ADHD (1957- Present

The 1960s saw ADD/ADHD, many multifaceted conditions separated and lumped under Minimum Brain Disorder (MBD).

The first diagnosis of ADD/ADHD was described in the Diagnostic and Statistical Manual of Mental Disorders (DSM Version II), naming ADD/ADHD as a genuine affliction under the name Hyperkinetic Reaction in Children in 1968.  Ross & Ross 1976 discovered that this did nothing to dispel the etiology (causation) concerning the condition’s classification as a behavioral or brain disorder.

Additional Theories postulated that ADD causation was caused by a neurochemical imbalance in the brain presented in 1970, resulting in yet another label: Catecholamine Hypothesis. Catecholamine Hypothesis came about from observing corrections in behavior in ADHD children given stimulant medication.

When DSM-III was published in 1980, Hyperkinetic Reaction in Children was changed to Attention Deficit Disorder (ADD), and again to Attention Deficit Hyperactivity Disorder (ADHD) in 1981. First coined in 1981 by Schachar, ADHD and ADD were defined in DSM-IV, published in 1994.

By 1970, researchers concentrated on the ADHD trilogy of impulsivity, inattentiveness, and hyperactivity when studying ADHD. Still, according to Palmer & Finger, it wasn’t until 1972 that researchers began to postulate that it was the inattention factor that was universally present in workers with ADHD.

Between 1980 and 1997, a wealth of research linking ADHD with Learning Disabilities and Executive Function Disorders (EFDs) in children linked ADHD with genetics as a possible vehicle for transmission.

A study in 2002 presented lowered dopamine levels in ADHD workers as a trigger for ADHD when researchers discovered neurochemical pathology of mental disorders based on drug mechanisms of actions. Since 2002, reduced dopamine levels in children and adults have proven consistent with ADHD symptomology.

ADHD became a household topic in the 1980s when the popular television news program “20:20” began airing a series on ADHD in children, resulting in more than 5,000 original articles and studies published during the next 25 years!

Even though Electroencephalographs (EEGs) came out in 1924, it wasn’t till 2010 that EEG saw its first use in ADHD research. Baumeister & Henderson discovered that brain wave plots from ADHD children showed abnormal EEGs. Brain wave research led to the Golden Age of ADHD research as hundreds of studies connecting ADHD to focal lesions and frontal lobe abnormalities were published and later refuted when more advanced tools such as Magnetic Resonance Imaging (MRI) became available.

In 2011, a study by  Asherson discovered the relationship between ADHD and criminal behavior, connecting ADHD with increased risks of psychopathological conditions. While Asherson’s data from these studies are compelling, none included variables such as isolationism from predatory discrimination or dysfunctional family environments.

Why is ADHD A Moving Target

Even among medical practitioners, the validity of ADHD is uncontested.  According to Baumeister & Henderson, what is contested is whether ADHD is a Neurobiological, Psychiatric, or Neurobehavioral disorder because of our inability to pinpoint causality. One side argues that ADHD is neurobiological and has been around for a long time, while the other side argues that modern society created ADHD, either physically or socially, so it must be a neuropsychiatric condition.

The most recent research has mostly settled this perplexing question by implicating more than 50 genes involved with ADHD. More genes are expected to be implicated as new diagnostic tools and research become available. Genetic research completed by Comings within the last decade suggests that ADHD is polygenic, meaning ADHD includes many components or symptoms.

As more adults are diagnosed with ADD/ADHD, heredity plays a major role in more than 80% of recently diagnosed ADHD adults.  Unfortunately, even this is a bit confusing as ADHD can be present in consecutive generations or can jump generations. As if the origin of ADHD wasn’t confusing enough, Comings found that environmental factors affect genetics in complex ways, suggesting several types of ADHD.

The American Psychiatric Association’s redefining ADD/ADHD in all four versions of the Diagnostic and Statistical Manual of Mental Disorders (DSM II-IV). Hasn’t helped to settle the ADD/ADHD controversy.  Comings indicate that DSM Volumes II through IV have three dominant types of ADHD: ADHD-I being the inattentive type, ADHD-H being the hyperactive type; and ADHD-C being a combination of inattentive and hyperactive types. Limited primarily to children, the hyperactive component is present in one to two percent of adults diagnosed with ADHD.

The scattering of comorbid components across the adult ADHD spectrum seems to refute a single constant until Executive Function Disorders (EFDs) are considered. According to Bedrossian, public polls listed EFDs as the most salient and visible form of ADHD, including the EFD conditions of Poor frustration tolerance, inability to plan, disorganized judgments, emotional expressions, and lack of inhibition. These EFD conditions are descriptive across the entire adult ADD/ADHD population. While this list is undoubtedly incomplete, it presents the list of EFDs most often associated with ADHD.

Biederman describes a paper by the Director of the Woodward Clinic Center for Mental Health Research and Treatment in Sherbrooke, Quebec, by suggesting that although ADHD appears to follow children through adolescence and into adulthood, it is a somewhat modified form of ADHD. The paper failed to take into consideration the abilities of ADHD adults to adapt and overcome many of ADHD’s most salient comorbid components, or this paper might appear plausible. A study completed by Nelson, Rinn, & Hartnett in 2006 refutes the paper by showing that many workers who went through the earliest stages of neurocognitive training exhibited few to no ADHD symptoms after completing the training.

Conclusion

If you made it this far without falling asleep, I commend you! As you can see, the meandering history of ADHD’s false starts in diagnosis and treatments, the constantly redefining ADHD, and studies refuting earlier studies have provided enough fodder for news agencies to blow ADHD entirely out of proportion. As a result, Q Public’s opinion of ADHD follows the latest iteration of irresponsible news media intent on sensationalizing ADHD for profit.  With this in mind, I have extensively researched ADHD to bring you the latest information on ADHD.

As you continue your search for how ADHD impacts your life and that of a loved one or friend, you will find a wealth of information proving you are not alone! Those of us who suffered from ADD/ADHD in the 1940s and ’50s did so silently because there was little to no information available to the public or schools.  We had to conclude why we were so different from everyone else in the only way we could by assuming we just weren’t as smart as everyone else, which eventually proved just the opposite!

Over 60% of adults diagnosed with ADHD as children will continue to have problems associated with ADHD throughout adulthood.  Some, but not all, related behaviors include emotional, social, vocational, and academic issues. ADHD is a lifelong condition inherited from at least one parent, who may not even know they have ADHD. While the belief that ADHD is a lifelong condition is prevalent today, there is enough controversial literature to shroud the subject in doubt. News agencies are capitalizing on sensationalizing questions and outliers resulting from research on ADHD within the family unit and workplace!

Within the United States, almost eight percent of children and five percent of adults are diagnosed with ADHD, with another four percent of the adult population either not knowing they have ADHD or thought they outgrew ADHD when they reached adulthood. The number suggested in a study completed in 2012 by Asherson was that 65% of ADHD children continue to be impaired by ADHD into adulthood. These numbers equate to nine million adults with ADHD in the United States alone!  To put this into perspective regarding intrinsic value in the workplace, Human Resources research by Coetzer & Richmond shows that ADHD generates $19.5 billion in lost human capital annually!

To a large degree, adults diagnosed with ADD/ADHD beyond the age of 30  discovered the fact in one of two ways: A child was diagnosed with ADD/ADHD, and a parent equates the child’s symptomology with their own, or someone close to them suggested they might have ADD/ADHD.

Unfortunately, ADHD in Education has not advanced nearly as fast as recent studies suggest, resulting in a growing number of ADHD students left behind as collateral damage, resulting in a burgeoning incarcerated population! Teachers, the unsung heroes of today’s education, do their best in the vacuum of available training on handling ADHD students, but alas, I’m getting ahead of myself. ADHD education is a subject for another page…

I hope you’ve gained insights from this history of ADHD, and I hope you continue to investigate more about ADHD as I publish additional pages on this website.

Introduction To The History Of ADHD

Welcome to the History of ADHD Timeline. While the history of ADHD is not the most exciting subject, it is necessary to answer the question: “Why do some folks say ADHD is not a real condition?” To answer this question, we must go back to the beginning, when the condition we know as ADHD was first observed, noted, and treated.

As you read through the History of ADHD, you will find many reference notations. If you wish to read the entire study, following this history is the complete reference. To be forewarned, some of these studies are hundreds of pages long!

 The History Of ADHD (1798-1944)

ADHD has undergone more iterations, evolutions, and convoluted twists and turns than any other condition afflicting humans (Stein, 2013). First described as a disturbance of brain nerves in 1798 by Baumeister and Henderson, ADHD has undergone a lengthy evolution of descriptions and diagnostic criteria. The name for the condition has changed no less than a half dozen times, as have descriptions and treatment options according to mental health professionals during the past two hundred plus years. According to Orendorff in 2009, this historical meandering of ADHD’s diagnostic history is perhaps what leads us to the present-day question: “Does ADHD exist?

The hypothesis of two prominent causes for ADHD was presented in 1902 by Tredgold; Brain Cell Metabolism and Defects in Moral Control. The encephalitis pandemic of 1917-1918 (Encephalitis is inflammation of the brain) resulted in several studies on ADHD, including Tredgold’s analysis of Neurological Orientation. Tredgold postulated that rather than the trilogy of impaired attention, hyperactivity, and poor impulse control, the cause for the condition was Social Moral Decay. Tredgold also hypothesized that impaired concentration was associated with physiological components resulting from disease or injury to further muddy the water. Interestingly, Baumeister and Henderson discovered that Tredgold’s and Crichton’s studies, separated by roughly 178 years, arrived at the same conclusion: ADHD had a neurobiological origin. 

Further support for Tredgold’s hypothesis came from studies from the post-Encephalitis Pandemic of 1917-1918 when children who survived the Encephalitis outbreak exhibited the same symptoms. This cluster of symptoms—poor impulse control, hyperactivity, and inattention became known as the Holy Trinity of ADHD. Tredgold’s study led to much interest within the medical and scientific communities, as additional studies were published that investigated links between ADHD and birth trauma, childhood measles, and head trauma. 

Studies following the Encephalitic Pandemic of the 1920s pointed to encephalitis as the cause of ADD, with three more labels connecting Encephalitis with ADD (Attention Deficit Disorder): Basal Ganglia Damage in 1929, Brain Stem Damage in 1931, and Brain-Stem Lesions in 1934.

In 1937, Dr. Charles Bradley performed Spinal Taps on children with the condition to research abnormalities in spinal fluid, resulting in severe headaches in the studied children. To alleviate these intense headaches, Dr. Charles Bradley administered stimulants. To his surprise, reports arrived over the next several days suggesting the general disposition of the ADHD group had improved significantly, and they were behaving like normal children in the class. During this same period, ADHD saw its first implication in girls, described by teachers and parents as having schizoid episodes. According to Schachar, Rtrrrer, & Smith, in 1981, a follow-up study involving the administration of stimulant medication to alleviate symptoms of ADHD saw similar results from the boys. 

In 2001, Palmer & Finger discovered laboratory studies in the 1940s involving animals with frontal lobe lesions that strengthened the relationship between ADHD and the pathological brain changes resulting from Restless Brain Syndrome. Restless Brain Syndrome studies continued to drive research well into the 1950s and 1960s with two new labels given to the condition: Minimal Brain Damage and Minimal Brain Dysfunction, both with the acronym MBD.

A period of concentrated studies followed the release of the synthesized stimulant medication Ritalin in 1944. This period of focused research would continue to ramp up exponentially between 1944 and 2014. A compilation of studies performed by Baumeister and Henderson discovered that between 1957 and the early 1980s, Seizures, Deficient Cortical Inhibition of Subcortical Structures, and lower Intelligence Quotient (IQ) levels were connected with ADD/ADHD.

The History Of ADHD (1957- Present

The 1960s saw ADD/ADHD, many multifaceted conditions separated and lumped under Minimum Brain Disorder (MBD).

The first diagnosis of ADD/ADHD was described in the Diagnostic and Statistical Manual of Mental Disorders (DSM Version II), naming ADD/ADHD as a genuine affliction under the name Hyperkinetic Reaction in Children in 1968. In 1976, Ross & Ross discovered that this did nothing to dispel the etiology (causation) concerning the condition’s classification as a behavioral or brain disorder.

Additional Theories postulated that ADD causation was caused by a neurochemical imbalance in the brain, resulting in another label: Catecholamine Hypothesis. Catecholamine Hypothesis came about from observing corrections in behavior in ADHD children given stimulant medication.

When DSM-III was Published in 1980, DSM-III changed the title Hyperkinetic Reaction in Children to Attention Deficit Disorder (ADD). 

First coined in 1981 by Schachar, ADHD and ADD made it into DSM-IV, published in 1994.

By 1970, researchers concentrated on the ADHD trilogy of impulsivity, inattentiveness, and hyperactivity when studying ADHD. Still, according to Palmer & Finger, it wasn’t until 1972 that researchers began to postulate that it was the inattention factor that was universally present in workers with ADHD.

Between 1980 and 1997, a wealth of research linked ADHD with Learning Disabilities and Executive Function Disorders (EFDs) in children, linking ADHD with genetics as a possible vehicle for transmission.

A study in 2002 presented lowered dopamine levels in ADHD workers as a trigger for ADHD when researchers discovered neurochemical pathology of mental disorders based on drug mechanisms of actions. Since 2002, reduced dopamine levels in children and adults have proven consistent with ADHD symptomology.

ADHD became a household topic in the 1980s when the popular television news program “20:20” began airing a series on ADHD in children, resulting in more than 5,000 original articles and studies published during the next 25 years!

Even though Electroencephalographs (EEGs) came out in 1924, it wasn’t till 2010 that EEG saw its first use in ADHD research. Baumeister & Henderson discovered that brain wave plots from ADHD children showed abnormal EEGs. Brain wave research led to the Golden Age of ADHD research as hundreds of studies connecting ADHD to focal lesions and frontal lobe abnormalities were published and later refuted when more advanced tools such as Magnetic Resonance Imaging (MRI) became available.

A study in 2011 by Asherson discovered the relationship between ADHD and criminal behavior, connecting ADHD with increased risks of psychopathological conditions. While Asherson’s data from these studies are compelling, the studies failed to include variables such as isolationism from predatory discrimination or dysfunctional family environments.

Why is ADHD A Moving Target

Even among medical practitioners, the validity of ADHD is uncontested. According to Baumeister & Henderson, deciding whether ADHD is a Neurobiological, Psychiatric, or Neurobehavioral disorder is the question of the day concerning ADDADHD because of our inability to pin down causality. One side argues that ADHD is neurobiological and has been around for a long time. In contrast, the other side argues that modern society created ADHD, either physically or socially, so it must be a neuropsychiatric condition.

The most recent research settled this perplexing question by implicating more than 50 genes involved with ADHD, proving a neurobiological disorder. More genes are expected to be implicated as new diagnostic tools and research become available. 

Genetic research completed by Comings within the last decade suggests that ADHD is polygenic, meaning ADHD includes many components or symptoms.

As more adults are diagnosed with ADD/ADHD, heredity plays a significant role in more than 80% of recently diagnosed ADHD adults. Unfortunately, even this bit is confusing as ADHD can be present in consecutive generations or can jump generations. 

As if the origin of ADHD wasn’t confusing enough, Comings found that environmental factors affect genetics in complex ways, suggesting several types of ADHD.

The American Psychiatric Association redefined ADD/ADHD in all four Diagnostic and Statistical Manual of Mental Disorders (DSM II-IV) versions, which hasn’t helped to settle the ADD/ADHD controversy. 

Comings indicate that DSM Volumes II through IV have three dominant types of ADHD: ADHD-I being the inattentive type, ADHD-H being the hyperactive type; and ADHD-C being a combination of inattentive and hyperactive types. The hyperactive component, Limited primarily to children, is present in one to two percent of adults diagnosed with ADHD. 

The scattering of comorbid components across the adult ADHD spectrum refutes a consistent element until Executive Function Disorders (EFDs) are added. According to Bedrossian, public polls listed EFDs as the most salient and visible form of ADHD, including the EFD conditions of Poor frustration tolerance, inability to plan, disorganized judgments, emotional expressions, and lack of inhibition. These EFD conditions are descriptive across the entire adult ADD/ADHD population. While this list is undoubtedly incomplete, it presents the list of EFDs most often associated with ADHD. 

Biederman describes a paper by the Director of the Woodward Clinic Center for Mental Health Research and Treatment in Sherbrooke, Quebec, by suggesting that although ADHD appears to follow children through adolescence and into adulthood, it is a somewhat modified form of ADHD. The paper failed to take into consideration the abilities of ADHD adults to adapt and overcome many of ADHD’s most salient comorbid components, or this paper might appear plausible. A study completed by Nelson, Rinn, & Hartnett in 2006 refutes the report by showing that many workers who went through the earliest stages of neurocognitive training exhibited few to no ADHD symptoms after completing the training.

Conclusion

If you made it this far without falling asleep, I commend you! As you can see, the meandering history of ADHD’s false starts in diagnosis and treatments, the constantly redefining ADHD, and studies refuting earlier studies have provided enough fodder for news agencies to blow ADHD entirely out of proportion. As a result, Q Public’s opinion of ADHD follows the latest iteration of irresponsible news media intent on sensationalizing ADHD for profit. With this in mind, I have extensively researched ADHD to bring you the latest information on ADHD. 

As you continue your search for how ADHD impacts your life and that of a loved one or friend, you will find a wealth of information proving you are not alone! Those of us who had ADD/ADHD in the 1940s and ’50s suffered in silence because there was little to no information available to the public or schools. We had to conclude why we were so different from everyone else in the only way we could by assuming we just weren’t as smart as everyone else, which eventually proved just the opposite!  

Over 60% of adults diagnosed with ADHD as children will continue to have problems associated with ADHD throughout adulthood. Some, but not all, related behaviors include emotional, social, vocational, and academic issues. ADHD is a lifelong condition inherited from at least one parent, who may not even know they have ADHD. While the belief that ADHD is a lifelong condition is prevalent today, there is enough controversial literature to shroud the subject in doubt. News agencies are capitalizing on sensationalizing questions and outliers resulting from research on ADHD within the family unit and workplace!

Within the United States, almost eight percent of children and five percent of adults are diagnosed with ADHD, with another four percent of the adult population either not knowing they have ADHD or thought they outgrew ADHD when they reached adulthood. The number suggested in a study completed in 2012 by Asherson was that 65% of ADHD children continue to be impaired by ADHD into adulthood. These numbers equate to nine million adults with ADHD in the United States alone! To put this into perspective regarding intrinsic value in the workplace, Human Resources research by Coetzer & Richmond suggests that ADHD generates $19.5 billion in lost human capital annually!

To a large degree, adults diagnosed with ADD/ADHD beyond the age of 30 discovered the fact in one of two ways: A child was diagnosed with ADD/ADHD, and a parent equates the child’s symptomology with their own, or someone close to them suggested they might have ADD/ADHD.

Unfortunately, ADHD in Education has not advanced as fast as recent studies suggest, resulting in a growing number of ADHD students left behind as collateral damage, resulting in a burgeoning incarcerated population! 

Teachers, the unsung heroes of today’s education, do their best in the vacuum of available training on handling ADHD students, but alas, I’m getting ahead of myself. ADHD education is a subject for another page…

I hope you’ve gained insights from this history of ADHD, and I hope you continue to investigate more about ADHD as I publish additional pages on this website.

Sincerely,
Dr. Terry L Southern
YouandMeandADHD.com

Drterry@youandmeandadhd.com

REFERENCES

Asherson, P., Akehurst, R., Kooij, J. J. S., Huss, M., Beusterien, K., Sasané, R., . . . Hodgkins, P. (2012). Under diagnosis of adult ADHD: Cultural influences and societal burden. Journal of Attention Disorders, 16(5 suppl), 20S-38S. doi:10.1177/1087054711435360

Baumeister, A., Hednerson, K., Pow, J., & Advokat, C. (2012). The early history of the neuroscience of attention-deficit/hyperactivity disorder. Journal of the History of the Neurosciences, 21(3), 263-279. doi:10.1080/0964704X.2011.595649

Bedrossian, L. (2011). Executive function’s role in ADHD issues shouldn’t be ignored. Disability Compliance for Higher Education, 16(11), 6-6.

Biederman, J. (2008). ADHD in adults: Current concepts and new developments. (Cover story). Canadian Journal of Psychiatry, 53(5), 1-4.

Coetzer, G. H., & Richmond, L. (2009). An empirical examination of the relationships between Adult Attention Deficit, Personal Task Management Systems and Role Stress. Journal of Behavioral & Applied Management, 10(2), 206-226.

Comings, D., Chen, T., Blum, K., Mengucci, J., Blum, S., & Meshkin, B. (2005). Neurogenetic interactions and aberrant behavioral co-morbidity of attention deficit hyperactivity disorder (ADHD): dispelling myths. Theoretical Biology & Medical Modelling, 2005(2), 50-65.

Nelson, J. M., Rinn, A. N., & Hartnett, D. N. (2006). The Possibility of Misdiagnosis of Giftedness and ADHD Still Exists: A Response to Mika. Roeper Review, 28(4), 243-248.

Orendorff, K. A. (2009). The relationship between ADHD and giftedness. Retrieved from http://search.ebscohost.com/login.aspx?direct=true&db=eric&AN=ED505127&site=eds-live&scope=site

Palmer, E., & Finger, S. (2001). An Early description of ADHD (Inattentive Subtype): Alexander Crichton and ‘mental restlessness’ (1798). Child & Adolescent Mental Health, 6(2), 66-73. doi:10.1111/1475-3588.00324

Ross, D., & Ross, S. (1976). Hyperactivity: Current issues, research, and theory. John Wiley & Sons Inc.

Sachjog-Velez, S. (2009). Relationships between executive functions, attention deficit hyperactivity disorder (adhd), comorbid disorders, and familial history in a nonclinical population. (PhD Dissertation), Philadelphia College of Osteopathic Medicine, Philadelphia. Retrieved from http://digitalcommons.pcom.edu/cgi/viewcontent.cgi?article=1142&context=psychology_dissertations  (143)

Schachar, R., Rtrrrer, M., & Smith, A. (1981). The characteristics of situationally and pervasively hyperactive children: implications for syndrome definition. Journal of Child Psychology & Psychiatry & Allied Disciplines, 22(4), 375-392. doi:10.1111/1469-7610.ep11742003

Stein, M. (2013). The war on ADHD. Nature Medicine, 19(12), 1566-1566. doi:10.1038/nm.3419

Waite, R. (2010). A Model for Parental ADHD: Help-Seeking and Readiness to Change. Issues in Mental Health Nursing, 31, 793-803.

Waite, R., & Ramsay, J. R. (2010). Adults with adhd: who are we missing? Issues in Mental Health Nursing, 31(10), 670-678. doi:10.3109/01612840.2010.496137

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