Background:
Attention deficit hyperactivity (ADHD) disorder is a neurodevelopmental
disorder characterized by inattention, hyperactivity, disruptive behaviour, and impulsivity. Despite
considered typical of children for a long time, the persistence of ADHD symptoms in adulthood
gained increasing interest during the last decades. Indeed, its diagnosis, albeit controversial, is rarely
carried out even because ADHD is often comorbid with several other psychiatric diosrders, in particular
with bipolar disorders (BDs), a condition that complicates the clinical picture, assessment and
treatment.
Aims:
The aim of this paper was to systematically review the scientific literature on the neurobiological,
clinical features and current pharmacological management of ADHD comorbid with BDs
across the entire lifespan, with a major focus on the adulthood.
Discussion:
The pharmacology of ADHD-BD in adults is still empirical and influenced by the individual
experience of the clinicians. Stimulants are endowed of a prompt efficacy and safety, whilst
non-stimulants are useful when a substance abuse history is detected, although they require some
weeks in order to be fully effective. In any case, an in-depth diagnostic and clinical evaluation of the
single individual is mandatory.
Conclusions:
The comorbidity of ADHD with BD is still a controversial matter, as it is the notion of
adult ADHD as a distinct nosological category. Indeed, some findings highlighted the presence of
common neurobiological mechanisms and overlapping clinical features, although disagreement does
exist. In any case, while expecting to disentangle this crucial question, a correct management of this
comorbidity is essential, which requires the co-administration of mood stabilizers. Further controlled
clinical studies in large samples of adult ADHD-BD patients appear extremely urgent in order to
better define possible therapeutic guidelines, as well as alternative approaches for this potentially
invalidating condition.
A novel homozygous variant in JAM3 gene causing hemorrhagic destruction of the brain, subependymal calcification, and congenital cataracts (HDBSCC) with neonatal onset