This 58-year-old male had PD for 20 years starting at the age of 38 years with resting tremor, bradykinesia and rigidity in his right hand. He had a negative history for drug or alcohol abuse as well as for psychiatric disorders. He had been successfully treated for 15 years at another medical center before coming to ours. When we first saw him, he was on pramipexol 1 mg tid, levodopa/carbidopa 1,000/200 mg/day and dispersible levodopa/benzerazide 50/12.5 mg tid In October 2006, pramipexol was increased to 4.5 mg/day and levodopa was replaced with levodopa/carbidopa/entacapone. Two years later, amantadine 100 mg tid was added for peak dose dyskinesias. In June 2009, he began to experience insomnia and simple visual hallucinations at sunset. He used to play cards when he was young, not for money, but he had been going to Bingo saloons for the last 3 years. Amantadine was discontinued and the hallucinations ceased, but he developed hypersexuality including aggressive behavior to his wife and sons, compulsive gambling with slot machines and severe insomnia. On one occasion he was found by one of his sons attempting to have sexual intercourse with a female family dog. He was also found to be taking several extra doses of pramipexol (up to 8 mg/day). He was put on quetiapine 50 mg and clonazepam 2 mg/day, and pramipexol was discontinued with marked improvement in behavior. Behavioral disorders associated with dopaminergic treatments are reward-based repetitive symptoms that promote pathological gambling, compulsive shopping and eating, punding, hypersexuality and compulsive medication use; this is known as dopamine dysregulation syndrome [1]. Our patient’s symptoms are consistent with those of DDS, but in addition, he has shown pathological gambling, hypersexuality, zoophilia, and insomnia, a well-known non motor complication of dopamine treatment. Zoophilia is more prevalent in men of low educational status, living in rural areas, as well as in psychiatric patients with mood disorders, substance abuse and anxiety [2]. The proposed mechanisms provoking these aberrant behaviors are the interactions between antiparkinsonian agents and D3 receptors expressed in the ventral striatal areas. It has also been proposed that dopaminergic therapy may affect sexual behavior through direct stimulation of D2 receptors in the medial preoptic area [3]. A further proposed mechanism is the inhibition of prolactin secretion by the stimulation of D2 receptors, increasing the plasma levels of oxytocin, which in turn, produces erectogenic effects in the lumbosacral spinal cord [3].

Deep brain stimulation of the subthalamic nucleus may either abolish or worsen hypersexuality [4]. In addition, a patient who undergoes a right pallidotomy may develop prominent hypersexuality after the surgical implantation of a deep brain stimulator electrode in the left globus pallidus [5]. Mendez et al.[6] described a patient who developed hypersexuality and paraphilic behavior after right pallidotomy.