Prefrontal cortex (PFC) represents one of the most evolved regions of primate brain that is thought to regulate human specific features such as cognition, emotion and behavior (Arnsten and Jin, 2012). PFC is a site of action of guanfacine, an agonist of alpha 2 adrenergic receptors. Compared to clonidine, another alpha adrenergic drug, guanfacine is more selective for α2A adrenergic receptor subtype (van Zwieten et al., 1994; Uhlen at al., 1995) and is weaker in producing hypotension andsedation (Jurado at al., 1998) resulting in better tolerability of the medication. Studies have shown that endogenous noradrenergic stimulation of alpha2A receptors is essential for PFC regulation of behavior, thought and emotion as blockade ofα2A receptors in the monkey dorsolateral PFC significantly impairs working memory (Li and Mei, 1994) and behavioral inhibition (Ma et al., 2003; Ma et al., 2003). So far FDA has approved guanfacine in treatment of attention deficit hyperactivity disorder in children but the medication is used off label for treatment of oppositional defiant disorder, conduct disorder, pervasive developmental disorders, motor tics and Tourette’s syndrome as well. Impulsivity as used in clinical terms is very broadly defined and encompasses personality traits as well as cognitive functions such as emotion regulation and behavioral inhibition. Numerous studies have shown effectiveness of extended release guanfacine in reducing impulsiveness in children with ADHD and recently in autism spectrum disorder (Scahill et al., 2015), however limited data is available on use of guanfacine in treatment of impulse control and aggression in adults.

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