Arch Gen Psychiatry. 2012 Jul 1;69(7):750-3
Authors: Edden RA, Crocetti D, Zhu H, Gilbert DL, Mostofsky SH
Abstract
CONTEXT Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by a deficit in behavioral inhibition. Recent evidence also suggests a deficit in cortical inhibition via the GABA (γ-aminobutyric acid)-ergic system.
OBJECTIVE To investigate the GABAergic component of ADHD using magnetic resonance spectroscopy.
DESIGN Cross-sectional study.
SETTING Participants were recruited through local schools, local pediatric and other community clinics, and through advertisement in regional publications. Magnetic resonance spectroscopy was performed within the research institute.
PARTICIPANTS Children (age range, 8-12 years) in a typically developing control group vs a group with ADHD were compared.
MAIN OUTCOME MEASURES J-difference-edited magnetic resonance spectroscopy at 3 T was used to measure GABA concentration in a volume that included primary somatosensory and motor cortices.
RESULTS GABA concentration is reduced in children with ADHD compared with typically developing control subjects.
CONCLUSION Our finding of reduced GABA concentration in ADHD is concordant with recently reported deficits in short intracortical inhibition in ADHD and suggests a GABAergic deficit in ADHD.
PMID: 22752239
Interestingly, some patients with ADHD respond better to an anxiolytic benzodiazepine like Clonazepam in improving attention than to a stimulant.
Some may need a benzodiazepine to ameliorate the negative effects of norepinephrine signaling under stimulant treatment, while keeping stimulant-increased dopamine signaling intact.
GABA is one of the control signals of brain cell norpepinephrine release.
Stimulants increase norepinephrine signaling.
Norepinephrine signaling is increased in many forms of ADHD. Norepinephrine is increased in production in response to various factors including metabolic impairments, internal and external stresses. The GABA loss in these patients is secondary to an increase in norepinephrine signaling.