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. 2021 Jan 25;14:590379. doi: 10.3389/fnhum.2020.590379

Table 1.

Timeline of events.

Time Event Description
35 years before admission The onset of Major Depressive Disorder (MDD) and panic attacks. Since the age of 20.
30 years before admission Panic attacks resolved with medication.
~28 years before admission Patient report of alcohol abuse and dependence. Patient attempt to “self-medicate” mood.
7 years before admission Vagus Nerve Stimulator (VNS) implanted for treatment-resistant MDD.
3 years before admission Received Electroconvulsive Therapy (ECT). Tolerated 2 sessions with mild post-ECT confusion; encephalopathic, confused and disoriented for 5 days after 3rd session. ECT stopped.
2 years before admission VNS device explanted. Due to lack of efficacy.
2 years before admission Deep Brain Stimulator (DBS) implanted for treatment-resistant MDD. Bilaterally in ventral internal capsule/ventral striatum; positive response for ~2 years.
~1–2 years before admission Patient scanned with Positron Emission Tomography (PET). In the context of a neuroimaging research study; inhaled radiolabeled CO2 molecules. Images acquired while stimulating at different DBS electrode positions.
16 weeks before admission Depressive symptoms worsened; resumed drinking up to four mixed drinks per day.
11 weeks before admission Radioablative treatment for lumbar spondylosis.
2 weeks before admission The onset of the patient presenting complaints. Brief episodes (20 s-2 min) of garbled nonsensical speech with paraphrasias, neologisms, agrammatism, coprolalia, rushes of anger and anxiety without panic symptoms, motor automatisms on the right arm and right leg.
1 day before admission The patient contacted the psychiatric neurotherapeutics team with presenting complaints. The patient advised to turn the DBS device off and present it to the clinic.
Admission The patient was seen at the outpatient clinic, referred to the Emergency. Department, admitted to Neurology service. DBS device turned off, normal neurological exam.
During admission Negative work up for TIA/stroke with CT of the brain, CTA of brain and neck, TTE, and 24 h Holter.
Normal limits for lipid panel, hemoglobin A1C, Vitamin B12, Thiamine, TSH, urine drug screen, blood alcohol level.
Negative work up for seizures with EEG when DBS device was off (and later on).
Two possible but unclear events with no epileptiform activity during 24 h long-term monitoring EEG.
DBS device turned on at original settings. Short episodes of progressively faster and louder stuttering with coprolalia, neologisms, agrammatism, paraphrasias, right-sided tic-like motor automatisms, ego-dystonic “rush” of physical and psychological activation; the patient had minimal memory of these events after they occurred.
The psychiatric neurotherapeutics team consulted. The voltage of the DBS device increased from 7 to 8 V with no changes, then increased to 8.5 V. The event started immediately and ceased when the voltage was reduced to 7 V.
Discharge Patient discharged and scheduled to follow up with neurotherapeutics team.
1 day after discharge The patient presented back at the outpatient clinic. DBS device turned on. Decreased pulse width to 90 μs of the left electrode, voltage left at 9V. The Patient reported no side effects and left with a safety plan.
3 weeks after discharge The patient called the neurotherapeutics team. Reported having a few brief similar episodes; advised to turn the stimulator off.
The patient returned to the outpatient clinic. Outpatient EEG with DBS device on at a higher intensity led to immediate induction of an event; no signs of epileptiform activity seen; EEG remained unchanged even when intensity reduced and behavioral effects disappeared.
DBS device turned on and left at same low pulse width (90 μs) but with reduced voltage (5 V).
Active leads on left stimulator were changed to a more dorsal position to match the position of right stimulator active leads; voltage slowly titrated up to 7.5 V bilaterally over several weeks.
No side effects have since been reported but depressive symptoms worsened and the patient lost initial beneficial response to DBS.