Mental or Made Up Illness ?? [Archive] - ADHD Forums - Attention Deficit Hyperactivity Disorder Support and Information Resources Community

scuro

05-27-05, 03:48 PM

I have just read another thread on mental illness and I thought I would share, I just recently went to a lecture on mental illness and it was said that ADHD is a made up illness. Where did this come from ???
N

Nockey- Scientology, and the Antipsychs which are led by Dr. Breggin and Dr. Baughman put great energy into trying to make the world believe that ADHD does not exist. Problem is they are not Scientists and really have no basis to make that claim. Dr. Russell Barkley is a Scientist and has devoted his life to prove that ADHD does exist. Read the link above.

Here is the history of ADHD also from the link above.

"Literary references to individuals having serious problems with inattention, hyperactivity, and poor impulse control date back to Shakespeare, who made reference to a malady of attention in King Henry VIII. A hyperactive child was the focus of a German poem, “Fidgety Phil,” by physician, Heinrich Hoffman (see Stewart, 1970). William James (1890), in his Principles of Psychology, described a normal variant of character that he called the “explosive will” that resembles the difficulties experienced by those who today are called ADHD. But, more serious clinical interest in ADHD children first occurred in three lectures of the English physician George Still (1902) before the Royal Academy of Physicians.

Still reported on a group of 20 children in his clinical practice whom he defined as having a deficit in “volitional inhibition” (p. 1008) that led to a “defect in moral control” (p. 1009) over their own behavior. Described as aggressive, passionate, lawless, inattentive, impulsive, and overactive, many of these children today would be diagnosed not only as ADHD but also as having oppositional defiant disorder (ODD). Still’s observations were quite astute, describing many of the associated features of ADHD that would come to be corroborated in research over the next century: (1) an overrepresentation of male subjects (ratio of 3:1 in Still’s sample); (2) high comorbidity with antisocial conduct and depression; (3) an aggregation of alcoholism, criminal conduct, and depression among the biological relatives; (4) a familial predisposition to the disorder, likely of hereditary origin; (5) yet with the possibility of the disorder also arising from acquired injury to the nervous system.

Interest in these children arose in North America around the time of the great encephalitis epidemics of 1917–1918. Children surviving these brain infections had many behavioral problems similar to those comprising contemporary ADHD (Ebaugh, 1923; Hohman, 1922; Stryker, 1925). These cases and others known to have arisen from birth trauma, head injury, toxin exposure, and infections (see Barkley, 1998) gave rise to the concept of a brain-injured child syndrome (Strauss & Lehtinen, 1947), often associated with mental retardation, that would eventually become applied to children manifesting these same behavior features but without evidence of brain damage or retardation (Dolphin & Cruickshank, 1951; Strauss & Kephardt, 1955). This concept evolved into that of minimal brain damage, and eventually minimal brain dysfunction (MBD), as challenges were raised to the label in view of the dearth of evidence of obvious brain injury in most cases (see Kessler, 1980, for a more detailed history of MBD).

By the 1950-70s, focus shifted away from etiology and toward the more specific behavior of hyperactivity and poor impulse control characterizing these children, reflected in labels such as “hyperkinetic impulse disorder” or “hyperactive child syndrome” (Burks, 1960; Chess, 1960). The disorder was thought to arise from cortical overstimulation due to poor thalamic filtering of stimuli entering the brain (Knobel, Wolman, & Mason, 1959; Laufer, Denhoff, & Solomons, 1957). Despite a continuing belief among clinicians and researchers of this era that the condition had some sort of neurological origin, the larger influence of psychoanalytic thought held sway. And so, when the second edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-II) appeared, all childhood disorders were described as “reactions,” and the hyperactive child syndrome became “hyperkinetic reaction of childhood” (American Psychiatric Association, 1968).

The recognition that the disorder was not caused by brain damage seemed to follow a similar argument made somewhat earlier by the prominent child psychiatrist Stella Chess (1960). It set off a major departure between professionals in North America and those in Europe that continues, to a lessening extent, to the present. Europe continued to view hyperkinesis for most of the latter half of this century as a relatively rare condition of extreme overactivity often associated with mental retardation or evidence of organic brain damage. This discrepancy in perspectives has been converging over the last decade as evident in the similarity of the DSM-IV criteria (see below) with those of ICD-10 (World Health Organization, 1994). Nevertheless, the manner in which clinicians and educators view the disorder remains quite disparate; in North America, Canada, and Australia, such children have ADHD, a developmental disorder, whereas in Europe they are viewed as having conduct problem or disorder, a behavioral disturbance believed to arise largely out of family dysfunction and social disadvantage.

By the 1970s, research emphasized the problems with sustained attention and impulse control in addition to hyperactivity (Douglas, 1972). Douglas (1980, 1983) theorized that the disorder had four major deficits: (1) the investment, organization, and maintenance of attention and effort; (2) the ability to inhibit impulsive behavior; (3) the ability to modulate arousal levels to meet situational demands; and (4) an unusually strong inclination to seek immediate reinforcement. Douglas’s emphasis on attention along with the numerous studies of attention, impulsiveness, and other cognitive sequelae that followed (see Douglas, 1983; and Douglas & Peters, 1978, for reviews) eventually led to renaming the disorder as attention deficit disorder (ADD) in 1980 (DSM-III; American Psychiatric Association, 1980). Significant, historically, was the distinction in DSM-III between two types of ADD: those with hyperactivity and those without it. Little research existed at the time on the latter subtype that would have supported such a distinction being made in an official and increasingly prestigious diagnostic taxonomy. Yet, in hindsight, this bald assertion led to valuable research on the differences between these two supposed forms of ADD that otherwise would never have taken place. That research may have been fortuitous, as it may be leading to the conclusion that a subset of those having ADD without hyperactivity may actually a separate, distinct, and qualitatively unique disorder rather than a subtype of ADHD (Milich, Ballantine & Lynam, 2001).

Even so, within a few years of the creation of the label ADD, concern arose that the important features of hyperactivity and impulse control were being de-emphasized when in fact they were critically important to differentiating the disorder from other conditions and to predicting later developmental risks (Barkley, 1998; Weiss & Hechtman, in press). In 1987, the disorder was renamed as attention-deficit hyperactivity disorder in DSM-III-R (American Psychiatric Association, 1987), and a single list of items incorporating all three symptoms was specified. Also important here was the placement of the condition of ADD without hyperactivity, renamed undifferentiated attention-deficit disorder, in a separate section of the manual from ADHD with the specification that insufficient research existed to guide in the construction of diagnostic criteria for it at that time.

During the 1980s, reports focused instead on problems with motivation generally, and an insensitivity to response consequences specifically (Barkley, 1989a; Glow & Glow, 1979; Haenlein & Caul, 1987). Research was demonstrating that under conditions of continuous reward, the performances of ADHD children were often indistinguishable from normal children on various lab tasks but when reinforcement patterns shifted to partial reward or to extinction (no reward) conditions, children with ADHD showed significant declines in their performance (Douglas & Parry, 1983, 1994; Parry & Douglas, 1983). It was also observed that deficits in the control of behavior by rules characterized these children (Barkley, 1989a).

Over the past decade, researchers employed information-processing paradigms to study ADHD and found that problems in perception and information processing were not so evident as were problems with motivation and response inhibition (Barkley, Grodzinsky, & DuPaul, 1992; Schachar & Logan, 1990; Sergeant, 1988; Sergeant & Scholten, 1985a, 1985b). The problems with hyperactivity and impulsivity also were found to form a single dimension of behavior (Achenbach & Edelbrock, 1983; Goyette, Conners, & Ulrich, 1978; Lahey et al., 1988), which others described as “disinhibition” (Barkley, 1990). All of this led to the creation of two separate lists of items and thresholds for ADHD when the DSM-IV was published later in the decade (American Psychiatric Association, 1994); one for inattention and another for hyperactive–impulsive behavior. Unlike its predecessor, DSM-III-R, the establishment of the inattention list once again permitted the diagnosis of a subtype of ADHD that consisted principally of problems with attention (ADHD predominantly inattentive type). It also permitted, for the first time, the distinction of a subtype of ADHD that consisted chiefly of hyperactive–impulsive behavior without significant inattention (ADHD, predominantly hyperactive–impulsive type). Children having significant problems from both item lists were titled ADHD, combined type. The specific criteria from DSM-IV are discussed in more detail below (see “Diagnostic Criteria and Related Issues”).

Healthy debate continues to the present over the core deficit(s) in ADHD with increasing weight being given to problems with behavioral inhibition, self-regulation, and the related domain of executive functioning (Barkley, 1997a, 1997b, 2000; Douglas, 1999; Nigg, 2001; Quay, 1997). The symptoms of inattention may actually be evidence of impaired working memory and not perceptual, filtering, or selection (input) problems (Barkley, 1997b). Likewise, controversy continues to swirl around the place of a subtype composed primarily of inattention within the larger condition of ADHD (see Clinical Psychology: Science and Practice, 2001, Vol. 8 (4) for a debate on this issue), with some arguing for it being a new, unique disorder from ADHD (Barkley, 2001; Milich et al., 2001) and others arguing that this distinction may be premature (Hinshaw, 2001; Lahey, 2001) or not especially important to treatment planning (Pelham, 2001). Relatively consistent across viewpoints, however, is the opinion that a subset of children having only high levels of inattention probably represents a qualitatively different problem in attention (deficient selective attention and sluggish cognitive processing) than is seen in ADHD (poor persistence, inhibition, and resistance to distraction)".