ADHD is not just a fad that has been created in the latter half of the 20th century. It is documented in history. In 493 B.C. Hippocrates, the great physician on the Greek island of Cos, described a condition in patients who had quick sensory experience and whose souls moved quickly on to the next impression. Believing that an imbalance of the four humors--water, fire, earth, and air--cause all diseases, Hippocrates attributed this condition to an over-balance of fire over water. He recommended a diet of barley rather than wheat bread and fish rather than meat; adding water, drinks, and natural and diverse physical activities were also recommended.

William Shakespeare, the famous British writer and poet, was a keen observer of behavior. He described how King Henry VIII had a serious malady of attention.

Thom Hartmann in his book Attention Deficit Disorder: A Different Perception proposes that ADD is a genetic disease that represents evolutionary survival strategies. Sickle cell disease, Tay-Sachs disease, and cystic fibrosis developed to protect people against certain diseases that were prevalent at the time. Hartmann argues that the attention deficit gene enabled those people in a hunting society to survive. The hunters have certain attributes, such as constantly monitoring the environment, thinking visually, and loving action, but hating mundane work; those characteristics made them successful. A failure to have the characteristics might have meant death in the forest.

History is full of references to people fitting the pattern of symptoms of inattention, restlessness, hyperactivity, and impulsivity. Hartmann said that in medieval Europe they possibly would be burned at the stake for being touched by demons. Native Americans might have elevated the person to greatness as a medicine man or shaman. He also questions what would have happened in history if Thomas Edison, Benjamin Franklin, Nostradamus, George Fredrick Handel, Salvatore Dali, Wolfgang Mozart, Ernest Hemingway, or Van Gogh had been medicated back to ''normal.''

As early as the 17th century, the philosopher John Locke described a perplexing group of young students who, try as hard as they could, would not keep their minds from straying. Abraham Lincoln's third son Tad was a holy terror in the White House, often chasing his brother through the Oval Office. Tad was reported to have major learning problems.

The German physician Heinrich Hoffman wrote one of the first references to a child with hyperactivity. In 1845 he penned a group of poems about the childhood problems that he saw in his practice; he called his character Fidgety Phil. Fidgety Phil did all the annoying things that one sees in a hyperactive individual, including leaning back in his chair and eventually pulling the table cloth off the table, causing all the food to land on the floor.

The first serious scientific studies of the phenomenon of inattention and hyperactivity are generally credited to George Still and Alfred Tredgold. In a series of three published lectures to the Royal College in 1902, Still described 43 children in his practice who had serious sustained attention problems. He referred to the philosopher/educator William James who said that paying attention is an important element in the classroom for the ''moral control of behavior.'' The children that Still described were often aggressive, defiant, resistant to discipline, and excessively emotional or passionate. According to Still, they showed little inhibitory control over their behavior and were also lawless, spiteful, cruel, and dishonest. They were insensitive to punishment and might continue a behavior, even though they were physically disciplined for it.

Still was convinced that these children displayed a major ''defect in moral control'' in their behavior and that they had perhaps acquired the condition as a secondary effect of an acute brain disease. He found the condition in 23 of his cases of children who were mentally retarded, but it also appeared in 20 children of near-normal intelligence. Some chronic cases developed into criminals, although not all. He concluded that a defect in moral control arose from three district impairments:

- A defect of cognitive relation to the environment

- A defect of moral consciousness

- A defect in inhibitory volition

Still observed that a greater proportion exist in males compared to females (3:1), and most cases appear before the age of 8. He observed that many of his patients had abnormal physical appearances, such as an abnormally large heads, malformed palates, or increased epicanthic folds over the eyelids. He called these deformities the ''stigmata of degeneration.'' These children had more accidents and were a threat to the safety of other children because of their aggressive or violent behavior. A study of their biological family trees showed the relatives displayed more alcoholism, criminality, and affective disorders such as depression.

According to Still's observations, some of the children displayed a history of brain damage or convulsions. A few had associate tic disorders or ''microkinesia''; this was the first time ADHD was possibly connected to comorbid conditions.

The family life of the children with hyperactivity played an important part in the development of Still's theories. Many of the children came from chaotic families, but others came from parents who seemingly tried to give the children a good upbringing. Still believed that when poor child rearing was involved, the children should be exempt from the category of lack of moral control; that belief was reserved for those who were raised in good families but still displayed morbid failure. For the children with good raising, he proposed possibly a hereditary condition or possibly pre- or postnatal brain injuries. He hypothesized that deficits in inhibition, moral control, and attention were all related to each other and to the same underlying neurological deficit. He also speculated about a syndrome where intellect was dissociated from the will and that condition might be a result of nerve cell modification. He also believed that temporary improvements might be found with changes in the environment or by using medications.

Alfred Tredgold in 1908 built on Still's idea that undetected damage accounted for the late-arising behavioral and learning deficiencies. Both of the physicians believed that the defect was permanent but could be helped by changes in the environment and possibly by medications. They strongly stressed the need for special educational environments. However, it would be 70 years before their ideas would take hold; the psychoanalytic and behavioral views overemphasized poor child rearing as largely causing such behavior disorders in children. Today, the children that Still and Tredgold described probably would be not only classified with ADHD but also with oppositional defiant disorder and most likely a learning disability.

The Great Influenza Pandemic of 1918 resulted in 650,000 deaths in North America. There were many complications of the flu that resulted in pneumonia and a brain disease called encephalitis. It was noted that many of the children who survived encephalitis had serious behavioral and cognitive deficits. Three papers by Ebaugh, Strecker, and Stryker appeared in the mid-1920s, which described children with symptoms that are currently ascribed to ADHD. The children were described as inattentive, impulsive, disorganized, memory deficient, and often socially disruptive. The condition was called ''postencephalitic behavior disorder'' and was clearly he result of brain damage. Many of the children were recommended for care outside of the home, and in spite of the view that these children were hopeless, some improved with simple behavior modification and increased supervision.

When the encephalitis epidemic appeared to cause changes in behavior manifestations, investigators explored the possibility of other causes of brain injury. In 1936, a study associated head trauma to attention deficit. This investigation led to later studies such as a 1938 study relating inattention and hyperactivity to epilepsy, a 1943 study relating the condition to lead toxicity, and a 1953 study correlating with measles. Terms describing the conditions during this era were ''organic driveness'' and ''restlessness'' syndrome. Many of the children in these studies had mental retardation, obvious brain damage, and more serious behavior problems than those associated today with ADHD, and decades elapsed before investigators began to separate the ideas of intellectual delay, learning disabilities, or other neurological deficits from those of the maladjustment in these children in earlier studies.

During this era researchers began to notice the striking similarity between hyperactivity in children and the behavior of primates with frontal lobe lesions. Some investigators had studied the frontal lobes of monkeys for more than 60 years, beginning when Ferrier published his study in 1876. He noted that the lesions in the frontal lobe resulted in excessive restlessness, poor ability to sustain interest in activities, aimless wandering, and excessive appetite. Levin in 1938 postulated that severe restlessness in children could be the result of defects in the forebrain structures, although he had little evidence to back up this conjecture. During this era, mild forms of ADHD were thought to be the result of poor parenting, which caused spoiled children, or of poor environment. This idea of poor parenting was resurrected in the 1970s and remains today among many lay people and critics of ADHD.

In the decade of the 1940s children who were hospitalized in facilities and who demonstrated attention deficit symptoms were assumed to have brain damage whether there was any evidence to support this idea. Strauss and Lehninen published a study using the term ''brain-injured child'' and applied it to those with problem behaviors. They even argued that the behavior was evidence of brain damage. In their classic text, these researchers recommended placing these children in smaller, more carefully regulated classrooms and reducing the amount of stimulation in the environment. For example, in this sterile and austere classroom, teachers could wear no jewelry or brightly colored clothing, and no pictures could be on the wall to distract students. This text was used as a guide to special education services adopted later in U.S. public schools. Many of the guidelines recommended in this text were incorporated into the initial Education for All Handicapped Children Act of 1975 (PL 94-142) mandating special education for children with learning disabilities and behavioral disorders and later in the Americans with Disabilities Education Act of 1990.

In the 1930s some researchers used pneumoencephalograms to study the brains of disruptive youths. This procedure involved injecting air into the brain and then using electrodes to trace brain patterns. To counteract headaches as a result of the experiments, the researchers gave the children drugs, especially amphetamines. They noted that both behavior and academic performance improved. In 1937 Dr. Bradley of Providence, Rhode Island, reported that a group of children with behavioral problems improved after being treated with stimulant medications. Later studies in the 1950s confirmed a positive response in half or more of hyperactive children when given amphetamines. Ritalin was first produced in 1950 and was initially used to treat narcolepsy, chronic fatigue, and depression and to counter the effects of other medications. By the 1970s stimulant medications were becoming the treatment of choice for behavioral symptoms now associated with ADHD. In 1996, the FDA approved a second medication, Adderall, for the treatment of ADHD. required less Metrazole to evoke a response than those without hyperactivity. The finding suggested that hyperactive children had a lower threshold for stimulation, possibly in the thalamic area. This study has never been replicated, and it would probably never pass an institutional review board for human experimentation. However, the study was a milestone in the history of the disorder because it indicated that a specific mechanism such as low cortical thresholds or over stimulation might give rise to the disorder. By the end of the 1950s it was generally accepted that hyperactivity was a braindamage syndrome, even when there was no evidence of actual damage.

In the late 1950s and 1960s critical reviews appeared questioning the concept of brain damage in those who displayed only the symptoms of hyperactivity. The idea of minimal brain disorder (MBD) was scrutinized. In 1966, a task force from the National Institute of Neurological Diseases and Blindness questioned applying the idea of brain damage and found at least 99 symptoms for the disorder. They proclaimed the idea as vague, over-inclusive, or of little or no prescriptive value. The term ''minimal brain disorder'' would die a slow death and be replaced by more specific and observable terms, such as dyslexia, language disorders, learning disabilities, and hyperactivity, designated ''minimal brain dysfunction.''

In 1960 Stella Chess urged researchers to focus on hyperactivity and defined the hyperactive child as one who carries out activities at a rate of speed that is higher than the normal rate of the average child or as one who is constantly in motion or both. Chess described the characteristics of 36 children from her practice that included 881 children and found that males outnumbered females in a ratio of 4 to 1. The children were referred before age 6, and educational difficulties were common. She also noted impulsive, aggressive behavior, and poor attention span. However, she maintained that the condition was relatively benign and that most children would outgrow it, but the ideas were important for the following four reasons:

1. Activity became the defining feature.

2. Objective evidence was considered beyond just the subjective reports of parents and teachers.

3. Blame was taken away from the parents.

4. The idea of hyperactivity was separated from the concept of brain damage.

In 1968, an important development in treatment occurred that seemed insignificant at the time. The second edition of the Diagnostic and Statistical Manual (DSM-II; American Psychiatric Association) added Chess's designation ''hyperkinetic reaction of childhood'' to its list of disorders. It used only one sentence to state that the disorder is characterized by restlessness, distractibility, overactivity, and short attention span, especially in young children. Taking the clue from Chess, writers of the manual stated that hyperkinetic disorder is a benign disorder that usually diminishes by adolescence.

By the end of this decade the prevailing idea was that hyperkinetic disorder was no longer ascribed to brain damage but instead, the focus was on brain mechanisms. The symptoms included a higher activity level than those displayed by a normal child. The condition was considered benign, with interventions to include short-term treatment with stimulant medications until it was outgrown in puberty. Classrooms were to provide little stimulation.

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