Psychosis from subthalamic nucleus deep brain stimulator lesion effect
A 47-year-old Caucasian man presented for STN DBS 5 years after his PD diagnosis. He reported no other medical problems. He had no prior psychiatric problems or family history of major mental illness, had quit tobacco over 20 years earlier, and used minimal alcohol. Like Mr. A, Mr. B had psychiatric side effects from pramipexole at doses above 4.5 mg daily. His personality had become more outgoing, he made inappropriate sexual comments, and he had a gambling addiction that prevented him from managing his own money. Despite these problems, he had experienced sufficient benefit that he had chosen to continue pramipexole. Neuropsychiatric testing 1 month before surgery was remarkable only for “minimal signs of depression” and nonspecific cognitive impairments suspected to be lifelong.\nMr. B presented for surgery early because PD was impairing his ability to work as a heavy equipment operator. His UPDRS Part III motor score 1 month before surgery was 37 off medication and 14 on medication. Prior to surgery, he was taking carbidopa-levodopa, clonazepam (for sleep), pramipexole, selegiline, and quetiapine (25 mg, for vivid dreams). The LED was 1600 mg.\nTarget AC-PC based coordinates for Mr. B were [x, y, z]: [-11.4, -2.8, -3.3 mm] on the left and [11.6, -2.7, -3.5 mm] on the right. STN-like activity on the left spanned 1.9 mm above to 1.7 mm below target, with arm movement related cells within 1 mm of target. Two guide cannulas were passed on the left, and three on the right. On the right, few cells were noted along the entire trajectory, although STN-like activity could be found from 0.24 mm above to 2.8 mm below target. One neuron that modulated its firing rate with hand grip was found at 0.24 mm above target. On both sides, Mr. B's rigidity improved substantially simply by electrode passage, and it was difficult to assess for further response to stimulation. Electrodes were placed with their distal contacts at 2.5 mm below target on both sides, as shown in Figures and . Transient paresthesias were elicitable at 2.6 V on the left, and as little as 2 V on the right during macrostimulation testing with the DBS electrode.\nPostoperatively, he was more somnolent than expected. EHU head CT done for lead placement verification[] showed a 3 × 9 mm right thalamic hyperdensity. After overnight observation, he was fully alert and oriented, and repeat CT showed no change in the thalamic hyperdensity. He discharged with only some right hand paresthesias. 1 week later, he reported some worsened dyskinesias and left upper extremity tremor, but no psychiatric symptoms. He had been able to slightly decrease his levodopa-carbidopa regimen, to an LED of 1525 mg.\nRepeat CT at 13 days postelectrode placement showed hemorrhage resolution, and he underwent generator placement the next day. His wife reported that since his 1-week checkup, Mr. B had become more impulsive and his gambling addiction had worsened. These symptoms were not attributed to his DBS, and he did not show any delirium or complications after generator placement, leading to discharge the same day.\nTwo days later (15 days postelectrode placement), on an international trip, he developed hypoverbality and a sense of near-continuous déjà vu. Selegiline was stopped. On return, when visiting his neurologist for evaluation, he became frightened and would not enter the appointment. By 19 days postelectrode placement, he was mostly nonverbal, but would have periods of hyperverbality and agitation. He ran away from our university ER when brought for evaluation, and had to be tricked into taking a dose of quetiapine and then rapidly driven back to the ER. He would not speak to the evaluating residents or remain in his room, although he did follow commands and comply with medical evaluation.\nMr. B's ER workup, including basic laboratory panels and another head CT (but not lumbar puncture) was unrevealing. He was admitted, and required a sitter to prevent him from leaving, but did not need physical restraint. Pramipexole was stopped, carbidopa-levodopa continued, clonazepam supplemented with lorazepam, and quetiapine repeatedly increased. He worsened, disclosing paranoid and grandiose delusions, although he remained fully oriented with an intact sensorium.\nMr. B markedly decompensated on the third hospital day (POD 22), when he developed visual hallucinations. He struggled against restraints so forcefully as to damage his hospital bed. At his most acute point, he had received a total of 150 mg quetiapine and 1.5 mg of IM lorazepam without effect, and refused further oral medication. IM olanzapine was considered unsafe due to the potential hypotensive interaction with lorazepam. After extensive deliberation and conclusion that the need to control an acute physical emergency outweighed the risks, 0.5 mg of haloperidol was given IV, and repeated roughly an hour later. This controlled his acute agitated state, and produced very minimal cogwheeling at wrists and ankles. He remained in restraints overnight, accepted more oral quetiapine at his wife's urging, and became calmer. He remained on his outpatient carbidopa-levodopa dose (1350 mg total) throughout these events.\nBy the following day, Mr. B no longer reported delusions or hallucinations and had calmed substantially. Over days 5 through 8 of his hospitalization, restraints were reduced, carbidopa-levodopa eliminated, and quetiapine given for agitation. He remained oriented, albeit concrete and without insight into his situation. He continued to have slight cogwheeling on passive extremity motion, but otherwise was without PD symptoms. At discharge on POD 27, he was in good behavioral control and his only medication was quetiapine, 350 mg daily.\nMr. B's DBS was activated and programmed at POD 55, and was uncomplicated [settings in ]. He returned to work and slowly tapered off quetiapine. He continues to show minimal PD symptoms at 2 years postsurgery, and has returned to both independent driving and his job operating heavy machinery.