Parkinson’s disease After Deep Brain Stimulation

The patient is a 54-year-old man who has had Parkinson’s disease since 1999 (age of onset 42). His initial symptoms were trouble manipulating his right hand, difficulty brushing his teeth, brushing his hair, shampooing his hair, and prior to that, Micrographia, related to the fact that his hand did not move very smoothly. His right arm swing was diminished, and he was dragging his right leg.

He was treated with Pergolide, followed by Mirapex, both of which lead to paranoid psychosis and obsessive behavior, as well as sleep problems, and ultimately, to psychiatric hospitalization.

The symptoms eventually cleared when the medications were removed. He ultimately required Carbidopa-Levodopa. Within a short time, he noticed the effects of the drugs wearing off and the symptoms included worsening of gait and severe painful Dystonia. The medications would last three hours or less. He also developed Dyskinesia. The Dyskinesia, Dystonia and gait disorder were severely disabling.

Upon initial evaluation, the patient had no cognitive symptoms except for an occasional “down” feeling. He reported no paranoia. In order to treat his motor fluctuations and Dyskinesia, the patient was treated with Catechol-O-methyltransferase Inhibitors, Monoamine oxidase inhibitors, Amantadine and clinical trial medication (Istradefylline), which only provided partial relief. Due to prior psychiatric issues, he was unable to retry Dopamine agonists. It was decided to treat him with deep brain stimulation surgery (DBS). The bilateral electrode placement into the subthalamic nuclei was performed on January 22, 2007. A pulse generator was placed February 12, 2007. Both procedures were accomplished without complications.

Initial programming was performed February 13, 2007. The patient was programmed in the off state. The settings after the first session were: On the right: 6- C+ 3.0 volts 60 microseconds and 134 Hz. On the left: 1- C+ 3.0 volts 60 microseconds and 130 Hz. At these settings, he had a dramatic improvement. His gait became normal, after being slow and shuffling. There was also increased agility in the upper extremities. Dyskinesia and Dystonia had, for the most part, disappeared. He has now been followed through 2010. While he maintains Carbidopa-Levodopa therapy, he continues to respond well to DBS. He has had no Dyskinesia and a 90 percent improvement of Dystonia. His primary symptom is slowness of movement when the Carbidopa-Llevodopa wear off. This is mild and he is still fully ambulatory and functions independently. He exercises regularly.