A 47-year-old, right-handed, Caucasian male presented for STN DBS 10.5 years after his initial PD diagnosis. He had no prior psychiatric history except depression that began as a symptom of PD. A pramipexole trial to 2.5 mg total daily dose had produced impulsivity, hypersexuality, jealousy, and compulsive gambling, which remitted after he stopped. He was a nonuser of tobacco, ethanol, or illicit drugs. He had no family history of major mental illness.
By the time of surgery, he had severe bilateral rigidity, painful dystonias, and persistent neck extension. His United Parkinson's Disease Rating Scale (UPDRS) Part III motor score before surgery was 48 off medication and 13 on medication. Medications prior to surgery were amantadine, carbidopa-levodopa, entacapone, selegiline, baclofen, escitalopram, and calcium carbonate. The levodopa equivalent dose (LED) was 3140 mg daily, calculated as per Tomlinson et al. He had substantial "wearing off" and disability even with this aggressive regimen. The risks and benefits of DBS were carefully weighed in Mr. A given his history of psychiatric complications. However, given his high level of disability and distress, the potential benefits were felt to have more weight. With his history of impulsivity with pramipexole, STN was selected as the DBS target to allow substantial reduction of his medication dosage.
Bilateral placement of STN-targeted DBS used initial coordinates chosen using a compromise between standard anterior commissure-posterior commissure (AC-PC) based coordinates, and coordinates relative to the borders of the red nucleus. Final planned coordinates were [x, y, z]: [-11.6, -3.5, -4.1 mm] on the left and [11.9, -3.6, -3.9 mm] on the right, relative to mid-commissural point and the AC-PC plane. Coordinates are not whole numbers as they reflect the rounding of corresponding Leksell frame-based coordinates to the nearest half-millimeter. Two guide cannulas were passed on each side. On the right, STN-like cellular activity was recorded from 2.6 mm above to 1.8 mm below the target, with modulation of firing rates with passive joint movement of the upper and lower extremity. Macrostimulation through a DBS electrode placed with its distal contact at 1.5 mm below target improved rigidity. On the left, STN activity spanned 3.8 mm above to 1.7 mm below target, with modulation with passive movement of right upper extremity. On this side also, the DBS lead was placed with distal contact 1.5 mm below target, with rigidity improvement during stimulation. Stimulation on both sides evoked transient paresthesias without dysarthrias at 1.5 V on the right and 4 V on the left. Intraoperative DBS positioning was confirmed using postoperative extended Hounsfield unit (EHU) computed tomography (CT) co-registered to preoperative magnetic resonance imaging (MRI) in standardized coordinates. This technique utilized both normalized mutual information (NMI) co-registration and manual paired-point anatomical registration methods to ensure there were no significant measurement errors due to brain shift. Whereas the NMI technique may favor co-registration of skull anatomy and thus not account for brain shift, the paired point registration provided verification by emphasizing anatomical structures such as the temporal horns, tectal plate, and trigeminal root entry. Atlas registration of final coordinates is shown in [Figure 1], with EHU CT-MRI imaging in [Figure 2] and coordinates for both patients in [Table 1].
Mr. A reported no major physical or mental symptoms postoperatively and underwent generator placement 1 week later without incident. Five days after generator placement (12 days post-DBS), he reported a robust microlesion effect, and reduced his medications to a LED of 1048 mg. He had no noticeable motoric side effects from this substantial decrease. Over the next 3 days, he became increasingly anxious, paranoid, and delusional, presenting twice to the emergency room (ER). Head CT, basic laboratory studies, and a lumbar puncture were all unremarkable. Amantadine, selegiline, and escitalopram were stopped, baclofen continued, and agitation treated with quetiapine. However, he continued to decline, making sexual comments toward nurses and refusing food. He remained fully oriented without hallucinations. Vital signs were normal.
Three days after admission, his agitation progressed to requiring physical restraints after he attempted violence against staff. He then refused all medications. After consideration of available options, he received 7.5 mg of intramuscular olanzapine against his will, which calmed him enough to engage in care and accept oral medications. Psychotic symptoms, including agitation, possible hallucinations, and impulsivity, persisted for at least a week more, up to POD 21. He did accept olanzapine 15 mg orally daily, plus his carbidopa-levodopa and entacapone. Starting on POD 22, he became apologetic for his behavioral outbursts, but retained memory for his actions. He continued to experience vivid dreams, but not waking hallucinations. He remained in the hospital on a psychiatric commitment until 15 days' hospitalization. Toward the end of this, he was cooperative with care, oriented, still apologetic, and entirely appropriate and coherent in his thoughts and speech.
He left the hospital on escitalopram (restarted), entacapone and carbidopa-levodopa (reduced dosing), and olanzapine 5 mg BID, with no signs of psychosis. By 3 months postdischarge, his only medications were carbidopa-levodopa, entacapone, and escitalopram (LED of 1064 mg). Stimulator programming/activation at POD 52 [settings in Table 2] did not cause new psychiatric symptoms, and he has remained psychiatrically stable for over 3 years. His pain and motor function have improved and he has expressed satisfaction with the surgery.