Methylphenidate-induced obsessive-compulsive symptoms: A case report and review of literature

Abstract

Literature on the association of methylphenidate and obsessive-compulsive symptoms (OCS) is sparse. This report discusses a case of a 14-year-old boy, who developed OCS (in the form of need for symmetry, obsessive doubts; compulsive symptoms included the need to order/arrange articles and repeated checking behavior), within 10 days of starting methylphenidate at the dose of 15 mg/day. Stoppage of methylphenidate led to amelioration of OCS over 2 weeks. The case description suggests that whenever a child on stimulants presents with new-onset OCS, association of OCS with stimulants must be suspected before considering an independent diagnosis of comorbid OCS/obsessive-compulsive disorder.

Co-Morbid Obsessive–Compulsive Disorder and Attention Deficit Hyperactivity Disorder: Neurobiological Commonalities and Treatment Implications

“…Some literature suggests that stimulants can exacerbate and provoke OCD symptoms. While this may be consistent with the theoretical understanding of dopaminergic prefrontal hyperactivity, this evidence is mostly anecdotal and remains limited (33–37).…”

Disruption of prepulse inhibition is associated with compulsive behavior severity and nucleus accumbens dopamine receptor changes in Sapap3 knockout mice

“…Our autoradiography results are consistent with PET/SPECT imaging studies demonstrating reduced D2/3 and D1 binding in striatum of OCD patients 15 , 16 , 19 . Compulsive behavior and disruption of PPI are both typically associated with a hyperdopaminergic state in striatum 13 , 21 – 25 , 45 . Given this, it is plausible that the observed correlations in Sapap3-KOs between severity of these OCD-relevant phenotypes and reduced dopamine receptor density may reflect compensatory downregulation of receptors in response to increased dopamine tone.…”

“…Specifically, increased cue-evoked striatal dopamine release has been observed via PET imaging in cocaine users, subjects with binge eating disorder, and patients with Parkinson’s disease who develop compulsive behavior following dopamine agonist treatment 21 – 24 . There is also evidence that drugs that increase dopamine signalling can exacerbate compulsive behavior in OCD patients 25 . Further supporting the role of elevated dopamine in the manifestation of OCD symptoms, dopamine antagonists can be useful as an adjunct therapy in OCD patients that don’t show clinical improvement following treatment with first-line selective serotonin reuptake inhibitors (SSRIs) 26 .…”

Disruption of prepulse inhibition is associated with severity of compulsive behavior and nucleus accumbens dopamine receptor changes in Sapap3 knockout mice

“…Our autoradiography results are consistent with PET/SPECT imaging studies demonstrating reduced D2/3 and D1 binding in striatum of OCD patients 15,16,19 . Compulsive behavior and disruption of PPI are both typically associated with a hyperdopaminergic state in striatum 13,[21][22][23][24][25]45 . Given this, it is plausible that the observed correlations in Sapap3-KOs between severity of these OCD-relevant phenotypes and reduced dopamine receptor density may reflect compensatory downregulation of receptors in response to increased dopamine tone.…”

“…Specifically, increased cue-evoked striatal dopamine release has been observed via PET imaging in cocaine users, subjects with binge eating disorder, and patients with Parkinson's disease who develop compulsive behavior following dopamine agonist treatment [21][22][23][24] . There is also evidence that drugs that increase dopamine signalling can exacerbate compulsive behavior in OCD patients 25 . Further supporting the role of elevated dopamine in the manifestation of OCD symptoms, dopamine antagonists can be useful as an adjunct therapy in OCD patients that don't show clinical improvement following treatment with first-line selective serotonin reuptake inhibitors (SSRIs) 26 .…”