Some case reports and a retrospective study state that methylphenidate (MPH) is effective in the treatment of encopresis that accompanies attention deficit/hyperactivity (ADHD). However, the mechanism of action related to these medications in the treatment of encopresis is not well-known. An eight-years-old male was referred to our clinic with complaints of encopresis that has been occurring almost every day for 2.5 years together with constipation. The patient had also experienced over activity, behavior, and concentration problems since he was three years old. He was assessed by a pediatrician before admission to our clinic, and neither pathological findings nor gastroenterological diseases, which could have explained the encopretic symptoms, were found except the constipation. The patient was diagnosed to have secondary encopresis (retentive type) and ADHD using the DSM-IV-TR criteria. Behavioral modifications for encopresis were planned, and 27 mg/d of long-acting methylphenidate (LA-MPH) was initiated. However, during the next visit, which was before the behavioral modifications were initiated, the encopresis, ADHD, and accompanying behavioral problems had disappeared, but the patient experienced irritability and loss of appetite with the LA-MPH medication. After eight months, due to irritability and appetite problems, 25 mg/d of atomoxetine (ATX) was added on the patient’s medications. Two months later, all the patient’s ADHD, oppositional behavior, and encopresis symptoms had disappeared, which prompted the clinic to stop the patient’s LA-MPH treatment. After the termination of the LA-MPH, encopresis occurred every day for a week, but the ADHD and oppositional behaviors did not. The child’s mother restarted the LA-MPH, and the encopresis disappeared again. In the present case, despite attention problems reduced via ATX, the encopretic symptoms did not. In our recent retrospective study in which patients were treated with MPH, no association between improvements in attention, hyperactivity, or behavioral problems and improvement in the encopretic symptoms occurred. In another case, a non-ADHD encopretic patient’s encopretic symptoms disappeared with LA-MPH. Therefore, MPH may have an effect on encopretic symptoms independent of ADHD symptoms. This case supports that assumption. Amphetamine, which has similar effects as MPH, was found to reduce the gastric emptying and intestinal motility via the D1 and D2 receptors in rats. Dopamine is effective in GIS motility, and the GIS contain the D1 and D2 receptors. Moreover, the GIS contains dopamine transporter (DAT), which is inhibited by MPH, and dopamine levels increase due to this inhibition. However, norepinefrine (NE) in the GIS does not originate from intrinsic enteric neurons; it originates from the enteric projections of extrinsic (sympathetic) neurons. The anti-encopretic effects of MPH may be related to its direct peripheral effects on GIS motility rather than its effects on executive functioning, self-organizing skills, or impulse control. Future studies investigating the peripheral effects of MPH on the GIS will improve the knowledge of this topic.