Despite the fact that my research lies at the intersection between cognitive, comparative, and developmental psychology, I am also quite interested in the evolution of our understanding of psychopathology. The ultimate goal of the study of psychopathology is to ground such disorders in brain and body. But our understanding of some pathologies are simply not there yet (though some of our therapeutic interventions still prove effective even if we don’t quite understand the etiology of a given disease or disorder). The main conflict in the field that characterizes the study of psychopathology is regarding the nature of psychopathology itself. Do psychological disorders reflect disease states superimposed onto otherwise healthy individuals? Or are psychological disorders wrapped up in personality and fundamental to the organization of a person? And to what extent does culture determine the extent to which we pathologize certain behaviors?
Complicated questions indeed. Consider the case of ADHD as a case study in the evolution of psychopathology.
What is ADHD? Paradigm Shifts in Psychopathology
Portions of this essay originally posted at Child’s Play
Over the last one hundred years, paradigm shifts in the study of psychopathology have altered our conceptualization of attention deficit/hyperactivity disorder (ADHD), as a construct and as a diagnostic category. With few exceptions, it has generally been accepted that there is a brain-based neurological cause for the set of behaviors associated with ADHD. However, as technology has progressed and our understanding of the brain and central nervous system has improved, the nature of the neurological etiology for ADHD has changed dramatically. The diagnostic category itself has also undergone many changes as the field of psychopathology has changed.
In the 1920s, a disorder referred to as minimal brain dysfunction described the symptoms now associated with ADHD. Researchers thought that encephalitis caused some subtle neurological deficit that could not be medically detected. Encephalitis is an acute inflammation of the brain that can be caused by a bacterial infection, or as a complication of another disease such as rabies, syphilis, or lyme disease. Indeed, children presented in hospitals during an outbreak of encephalitis in the United States in 1917-1918 with a set of symptoms that would now be described within the construct of ADHD.
In the 1950s and 1960s, new descriptions of ADHD emerged due to the split between the neo-Kraepelinian biological psychiatrists and the Freudian psychodynamic theorists. The term hyperkinetic impulse disorder, used in the medical literature, referred to the impulsive behaviors associated with ADHD. At the same time, the Freudian psychodynamic researchers (who seem to have won the battle in the DSM-II) described a hyperkinetic reaction of childhood, in which unresolved childhood conflicts manifested in disruptive behavior. The term “hyperkinetic,” which appears in both diagnoses, describes the set of behaviors that would later be known as hyperactive – despite the fact that medical and psychological professionals were aware that there were many children who presented without hyperactivity. In either case, it was the presenting behavior that was the focus – which was implicit, given the behavioral paradigm that guided the field.
When the cognitive paradigm became dominant, inattention became the focus of ADHD, and disorder was renamed attention deficit disorder (ADD). Two subtypes would later appear in the literature, which correspond to ADD with or without hyperactivity. The diagnostic nomenclature reflects the notion that the primary problem was an attentional (and thus, cognitive) one and not primarily behavioral. The attentional problems had to do with the ability to shift attention from one stimulus to another (something that Jonah Lehrer has called an attention-allocation disorder, since it isn’t really a deficit of attention). The hyperactivity symptoms were also reformulated as cognitive: connected with an executive processing deficit termed “freedom from distractibility.”
In DSM-IV, published in 1994, the subtypes were made standard and there wasn’t much change in the diagnostic criteria per se, but there were changes in the name of the disorder, which reflected changes in the literature in terms of the understanding of the etiology of the disorder. The term ADD did not hold up, and the disorder became known as ADHD, with three subtypes: ADHD with hyperactivity/impulsiveness, ADHD with inattention, and a combined subtype in which patients have both hyperactive and attention-related symptoms. Due to improved neuroimaging technology, these subtypes seem to reflect structural and functional abnormalities found in the frontal lobe, and in its connections with the basal ganglia and cerebellum.
The set of the symptoms associated with ADHD seem not to have changed much in the last one hundred years. However, paradigm shifts within the field of psychopathology have changed the way in which researchers understand the underlying causal factors, as well as which of the symptoms are thought to be primary.
Developmental Continuity in ADHD
Is there such a thing as adult ADHD?
In the DSM-IV-TR (and earlier versions of the DSM as well), attention deficit hyperactivity disorder (ADHD) falls under the superordinate category “Disorders First Appearing in Infancy, Childhood, or Adolescence.” Until the early part of the twenty-first century, many researchers and clinicians (and certainly the public) thought that children grew out of ADHD, and there was no adult variant. Some researchers have started to argue that there is, indeed, an adult variant of ADHD, and there is continuity in the disorder across development.
A key issue in the diagnosis of adult ADHD is the fear that adults could claim to suffer from the disorder as an excuse for otherwise unacceptable behavior. Connected to this is the fear among the general public that the pharmaceutical industry created the label ‘ADHD’ for kids who are simply disrespectful (think: Bart Simpson) or otherwise act inappropriately. However, in their well-regarded position paper, Barkley and colleagues described ADHD as a real disease-like state, and maintained that it was biologically defined and heritable.
The symptom profile for ADHD includes deficits in emotional regulation, irritability, peer rejection, and academic difficulties. Barkley describes a biological etiology for ADHD involving a heritable frontal lobe disorder that stays with an individual throughout development. What changes, then, must be are the symptoms associated with the underlying cause.
The main problem is that the diagnostic criteria for ADHD are normed for children, not for adults. The problem runs a bit deeper, however. ADHD has been conceptualized as a developmental disorder, which means that a pathological individual’s behavior must be inappropriate relative to his or her peers – and that behavior must somehow cause impairment in major life activities. This conceptualization assumes that individuals with a developmental disorder are merely behind their peers in the development of normal psychological traits, and not mal-developed. In order to define adult ADHD, diagnostic criteria must be used relative to other adults – this set of symptoms does not exist yet in the DSM. A complication is that the frequency of ADHD symptoms tends to decline with age. Unless the diagnostic criteria acknowledge this (and they don’t), then the number of individuals who fit within the diagnostic category with decrease through development.
Another piece of evidence for the developmental continuity of ADHD into adulthood comes from a 2002 study by Barkley, Fischer, Smallish, and Fletcher. Their thirteen-year longitudinal study found a low frequency of self-reported ADHD by the individuals themselves upon reaching adulthood. However, a far higher frequency was found when using parent reports (completed by parents of adult children). Not only were the parent reports more reliable, but they were also more valid: they were more strongly and pervasively associated with adversity in major life activities than were self-reports.
Taken together, the etiological continuity proposed by Barkley, the lack of sufficient norms for adult diagnosis of ADHD, and the psychometric continuity in parent reports, all point at least to the plausibility – if not the real existence – of adult ADHD as a valid diagnostic category, and therefore developmental continuity in the disorder.
Note: this post is part of a mini-carnival on the topic of psychopathology and mental illness. Check out all the other blogs that are participating!
Barkley, R. (2002). International Consensus Statement On ADHD Journal of the American Academy of Child & Adolescent Psychiatry, 41 (12) DOI: 10.1097/00004583-200212000-00001
Barkley RA, Fischer M, Smallish L, & Fletcher K (2002). The persistence of attention-deficit/hyperactivity disorder into young adulthood as a function of reporting source and definition of disorder. Journal of abnormal psychology, 111 (2), 279-89 PMID: 12003449