Abstract
Attention deficit hyperactivity disorder (ADHD) is a
common childhood neurodevelopmental disorder characterised
by age-inappropriate levels of inattention,
hyperactivity and impulsivity; and can persist into adulthood.
Adult ADHD increases the risks of anxiety,
depression, substance misuse and personality difficulties addition to educational, occupational, financial and
social impairments. Emotional dysregulation (ED) frequently
co-occurs with ADHD and can respond to
ADHD medications, paralleling ADHD core symptom
reduction. Notably, ED mediates the onset of subsequent
depression; and ADHD with a comorbid mood
disorder in adolescence increases the risk of completed
suicide by three-fold. This talk posits that ‘ADHD-ED’ is
a specific presentation that warrants focused research
and clinical attention; and provides some recent genetic
findings accounting for their association, in particular, a
twin study that decomposes the genetic architecture of
childhood ADHD and ED symptoms.
Furthermore, cumulative evidence suggests that ADHD
itself is a continuous spectrum disorder, with sub-threshold
cases carrying significant disease burden, to a degree similar
to those ‘subtypes’ recognized by DSM-IV and DSM5;
yet these sub-threshold cases are currently ‘diagnostically
homeless’. This talk argues for taxonomic recognition of
two diagnostically ‘lost tribes’:
1. Those of ‘ADHD + ED’; and
2. Those with diagnostically sub-threshold ADHDcombined
symptoms (i.e. ‘moderate combined
subtype’).
The third strand of this talk summarises some emerging
evidence that ADHD and autism co-exist as a phenotypic
continuum; and describes some clusters of syndromes
along this ‘ADHD-autism spectrum’. Furthermore, the
relationship between ED and oppositional defiance disorder
(ODD) symptoms will also be explored.
The fourth strand reviews neuroanatomical models for
ADHD-ED symptoms, while highlighting the relevant environmental
factors. More specifically, the ‘Dynamic Network
Connectivity’ (DNC) model describes unique neuromodulatory
influences on working memory prefrontal cortical
(PFC) circuits - mediated by D1, alpha 2A receptors and
HCN channels - and embodies novel pharmacological and
psychological treatment implications. The talk concludes
with some new directions for research and development.
common childhood neurodevelopmental disorder characterised
by age-inappropriate levels of inattention,
hyperactivity and impulsivity; and can persist into adulthood.
Adult ADHD increases the risks of anxiety,
depression, substance misuse and personality difficulties addition to educational, occupational, financial and
social impairments. Emotional dysregulation (ED) frequently
co-occurs with ADHD and can respond to
ADHD medications, paralleling ADHD core symptom
reduction. Notably, ED mediates the onset of subsequent
depression; and ADHD with a comorbid mood
disorder in adolescence increases the risk of completed
suicide by three-fold. This talk posits that ‘ADHD-ED’ is
a specific presentation that warrants focused research
and clinical attention; and provides some recent genetic
findings accounting for their association, in particular, a
twin study that decomposes the genetic architecture of
childhood ADHD and ED symptoms.
Furthermore, cumulative evidence suggests that ADHD
itself is a continuous spectrum disorder, with sub-threshold
cases carrying significant disease burden, to a degree similar
to those ‘subtypes’ recognized by DSM-IV and DSM5;
yet these sub-threshold cases are currently ‘diagnostically
homeless’. This talk argues for taxonomic recognition of
two diagnostically ‘lost tribes’:
1. Those of ‘ADHD + ED’; and
2. Those with diagnostically sub-threshold ADHDcombined
symptoms (i.e. ‘moderate combined
subtype’).
The third strand of this talk summarises some emerging
evidence that ADHD and autism co-exist as a phenotypic
continuum; and describes some clusters of syndromes
along this ‘ADHD-autism spectrum’. Furthermore, the
relationship between ED and oppositional defiance disorder
(ODD) symptoms will also be explored.
The fourth strand reviews neuroanatomical models for
ADHD-ED symptoms, while highlighting the relevant environmental
factors. More specifically, the ‘Dynamic Network
Connectivity’ (DNC) model describes unique neuromodulatory
influences on working memory prefrontal cortical
(PFC) circuits - mediated by D1, alpha 2A receptors and
HCN channels - and embodies novel pharmacological and
psychological treatment implications. The talk concludes
with some new directions for research and development.
| Original language | English |
|---|---|
| Pages | 2-3 |
| Number of pages | 2 |
| Publication status | Published - 2014 |
