The incapacity of attending with a necessary degree of constancy to any one object (Sir Alexander Crichton, 1763–1856)
The first example of a disorder that appears to be similar to ADHD was given by Sir Alexander Crichton in 1798. Crichton was a Scottish physician who was born in Edinburgh in 1763. In 1785, he received his M.D. from the University of Leiden, The Netherlands (Palmer and Finger 2001; Tansey 1984). He then decided “to undertake a European medical tour” (Tansey 1984, p. 243) and practiced in hospitals in Paris, Stuttgart and Vienna (Tansey 1984). In his clinical practice, Crichton observed many cases of insanity and became increasingly interested in mental illness (Palmer and Finger 2001). In 1798, he published “An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects”. In this work of three books, he demonstrated observations of clinical cases of mental illness (Palmer and Finger 2001). Up until the end of the eighteenth century, when Crichton published his inquiry, it was uncommon to focus on mental issues from a physiological or medical perspective (Palmer and Finger 2001). Crichton mentioned that at the time there were only two other authors who had “written fully on the subject of Mental Diseases” (Crichton 1798, pp. ii–iii, cited by Palmer and Finger 2001).
The second chapter of book II “On Attention and its Diseases” is of special interest to the present subject. Crichton begins this chapter with a definition of attention: “When any object of external sense, or of thought, occupies the mind in such a degree that a person does not receive a clear perception from any other one, he is said to attend to it” (Crichton 1798, reprint p. 200). Crichton emphasizes that the intensity of healthy attention varies within a normal range both between individuals and even within a person at different times (Crichton 1798). A distraction of attention does not necessarily have to be pathological, e.g. mental stimuli, volition, or education can have a great impact on healthy attention (Crichton 1798). Crichton distinguishes two possibilities of abnormal inattention as the oppositional poles of pathologically increased or decreased “sensibility of the nerves” (Crichton 1798):
The morbid alterations to which attention is subject, may all be reduced under the two following heads:
First. The incapacity of attending with a necessary degree of constancy to any one object.
Second. A total suspension of its effects on the brain.
The incapacity of attending with a necessary degree of constancy to any one object, almost always arises from an unnatural or morbid sensibility of the nerves, by which means this faculty is incessantly withdrawn from one impression to another. It may be either born with a person, or it may be the effect of accidental diseases.
When born with a person it becomes evident at a very early period of life, and has a very bad effect, inasmuch as it renders him incapable of attending with constancy to any one object of education. But it seldom is in so great a degree as totally to impede all instruction; and what is very fortunate, it is generally diminished with age. (Crichton, 1798, reprint p. 203)
Citation:(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3000907/)
Advances in the genetics of childhood neuropsychiatric disorders over the past decade were reviewed in the literature and reported from Yale University School of Medicine, New Haven, CT. In ADHD a genetic basis is suggested by family and twin studies. A focus on dopamine neurotransmission showed that children with ADHD had a higher incidence of the high-risk variant of DRD4 than controls, but the relationship is still controversial. The dopamine transporter gene (DAT1) has been linked to ADHD. Mice lacking expression of this gene were more active than control littermates. Functional variants of genes involved in dopamine transmission may confer a familial risk for ADHD. [1]
Parental ADHD. Weiss M, Hechtman L, and Weiss G provide a clinical perspective on ADHD in parents [2]. ADHD is highly familial. More than 50% of parents with ADHD have a child with ADHD, and 25% of children with ADHD have an ADHD parent. Siblings are frequently affected, and families with multiple ADHD members are especially challenged. Parents with ADHD are recognized for their failure to keep appointments for the child patient, they are restless in the office, they forget to bring along school reports, and they monopolize the interview. Parental ADHD can impact family functioning and the treatment of the child. Family counseling must address both the child’s and parent’s problems.
Executive functions and ADHD are reviewed by Barkley RA in Part 1 of a series of columns on the Genetics of ADHD [3]. The term executive function, deficient in ADHD, includes purposive, goal-directed activity; inhibition of distraction; response inhibition or delayed gratification; selective problem-solving; flexibility; goal persistence; and self-awareness. Self-regulation is essential for normal executive function. The prefrontal cortex is the anatomic localization of these functions. Attention deficits typical of ADHD are termed intention deficits.
Citation: ( Millichap, J.G., (2000). Genetics of ADHD. Pediatric Neurology Briefs. 14(8), pp.60–61. DOI: http://doi.org/10.15844/pedneurbriefs-14-8-7)
Heritability, family studies, suitability for genetic studies
Family and twin studies of cADHD demonstrate a high heritability, estimated to be around 70–80% from twin studies.6, 7 Relatively few studies have investigated the genetic and environmental contributions to the developmental course and outcomes in adulthood. Longitudinal twin studies show that the continuity of symptoms from childhood through to adolescence is predominantly due to common genetic influences.8, 9,10 Although such stable genetic effects are likely to continue beyond the adolescent years, there are only a few studies investigating this.
Genetic research on ADHD started with the finding that hyperactivity tends to aggregate in families.11, 12Since then, family studies have shown that ADHD shows familial clustering both within and across generations. Increased rates of ADHD among the parents and siblings of ADHD children have been observed.13, 14 In addition, strongly increased risks for ADHD (57%) among the offspring of adults with ADHD have been reported.15 Also, compared with the risk for ADHD among the siblings of children with ADHD (15%), siblings of adults with ADHD were found to have a strongly increased ADHD risk (41%).16Furthermore, a prospective 4-year follow-up study of male children into mid-adolescence found the prevalence of ADHD to be significantly higher among the parents and siblings of persistent ADHD child probands compared with the relatives of ADHD probands in whom ADHD remitted.17 Taken together, these studies suggest that the risk for ADHD may be greater among the first-degree relatives of probands with ADHD that persists into adolescence and adulthood than that among the relatives of probands with ADHD that remits before adulthood.17, 18
Whether such familial risks reflect genetic or environmental factors can be clarified using adoption and twin studies. Adoption studies found that ADHD is transmitted only to biological relatives, which strongly implicates genetic factors as the main causal influences on familial risk for the disorder.11, 12, 19, 20, 21These studies showed (for both current and retrospective symptoms in adults) that cADHD in child relatives predicts aADHD (or associated symptoms) in adult relatives. However, both adoption and family studies identify discrepancies related to different sources of ratings, with self-evaluation of ADHD symptoms by adults providing less evidence of familial effects than informants or cognitive performance data.19, 22, 23
Recently, four adult population twin studies using self-ratings of ADHD symptoms have been completed, which all found heritabilities that are far lower than those found in similar studies of parent- or teacher-rated cADHD: 41% for retrospectively reported childhood ADHD symptoms in a sample of 345 US veterans aged 41–58 years old,24 40% for current inattention problems in a Dutch study of 4245 18–30-year olds,8 30% for current ADHD symptoms in a Dutch study of over 12 000 twin pairs with an average age of 31 years25 and 35% for current ADHD in a Swedish sample of more than 15 000 twin pairs aged 20–46 years (Larsson et al., unpublished data). The situation is similar in adolescence, as adolescent twin studies using self-ratings show lower heritability estimates than studies of parent or teacher ratings,26, 27suggesting that self-ratings may be a poorer measure of the underlying genetic liability to ADHD than informant reports or clinical interviews. Although the estimated heritability in self-rated ADHD symptoms in adult populations is lower than that derived from parent or teacher ratings of cADHD, the pattern of findings is identical. Both types of studies find that there are no gender differences observed in the estimates of heritability, heritability estimates are stable across the age-span (for each type of measurement approach), there are similar estimates of the genetic correlation (the proportion of shared genetic effects) of 60–70% between inattention and hyperactivity-impulsivity, familial effects are all genetic in origin with no shared environmental influences, and no threshold effects are found. This suggests that for both child and adult ADHD the disorder is best perceived as the impairing extreme of a quantitative trait (Larsson et al., unpublished data; ref. 28).
Citation: (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3449233/)
