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Electroconvulsive therapy for depression in a Parkinson's disease patient with bilateral subthalamic nucleus deep brain stimulators
Parkinsonism and Related Disorders 11 (2005) 403–406 www.elsevier.com/locate/parkreldis
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Electroconvulsive therapy for depression in a Parkinson’s disease patient with bilateral subthalamic nucleus deep brain stimulators Kelvin L. Choua,*, Howard I. Hurtigb, Jurg L. Jaggib, Gordon H. Baltuchc, Rodney J. Pelchatd, Daniel Weintraubb,e a Department of Clinical Neurosciences, Brown University Medical School, Providence, RI, USA Parkinson’s Disease and Movement Disorders Center, Pennsylvania Hospital, University of Pennsylvania, Philadelphia, PA, USA c Department of Neurosurgery, Penn Neurologic Institute at Pennsylvania Hospital, University of Pennsylvania, Philadelphia, PA, USA d Department of Psychiatry, Jefferson Medical College, Philadelphia, PA, USA e Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA b
Received 4 February 2005; revised 5 April 2005; accepted 6 April 2005
Abstract We report a patient with advanced Parkinson’s disease (PD) who developed a recurrence of major depression with psychotic features after bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) surgery. Electroconvulsive therapy (ECT) dramatically improved the depression without shifting electrode position or damaging the DBS hardware. This case suggests that ECT can be a safe and effective option for severe depression in PD patients treated with STN DBS. q 2005 Elsevier Ltd. All rights reserved. Keywords: Parkinson’s disease; Deep brain stimulation; Subthalamic nucleus; Depression; Electroconvulsive therapy
1. Introduction Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective option for patients with advanced Parkinson’s disease (PD). STN DBS improves motor function, decreases dyskinesias, and reduces levels of dopaminergic medications [1,2]. However, several studies have suggested that STN stimulation can be associated with deleterious effects on mood, especially depression [3–7]. In many cases, depressive symptoms occur within a month post-operatively and resolve either without specific therapy or with minor stimulator adjustments [3,6,7], but depression after DBS surgery can occasionally be refractory to medical management and even result in suicide [5,7,8]. Electroconvulsive therapy (ECT) can be effective for treatment-resistant depression, even in patients with PD [9]. * Corresponding author. Address: Division of Neurology, Memorial Hospital of Rhode Island, 111 Brewster Street, Pawtucket, RI 02860, USA. Tel.: C1 401 729 3757; fax: C1 401 729 3101. E-mail address: [email protected] (K.L. Chou).
1353-8020/$ - see front matter q 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.parkreldis.2005.04.005
However, there is minimal experience with ECT in patients who have undergone DBS procedures [10]. We report a PD patient who developed a recurrence of a major depressive episode with psychotic features after implantation of bilateral STN DBS electrodes and was subsequently treated safely and successfully with ECT.
2. Case report This 66-year-old Greek woman presented with bradykinesia and tremor of the right arm in 1997 at the age of 59. She was diagnosed with PD and started on carbidopa/levodopa with significant benefit. However, classic motor fluctuations developed within 3 years, and dyskinesias became severely disabling. The addition of ropinirole (9 mg daily) and amantadine hydrochloride (200 mg daily) did not ameliorate fluctuations or dyskinesias. Levodopa, when optimally effective (in the ‘on’ state) , allowed her to be independent in all activities of daily living and to walk without an assistive device. During the wearing-off state, she experienced considerable bradykinesia and rigidity, and was unable to walk. Formal
404
K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
neuropsychological testing was not performed due to severe language barriers, but cognitive functioning had remained relatively unimpaired according to the family. She was considered a good candidate for surgery because of the prospect that the marked fluctuations and prolonged off-time would improve significantly. The past medical history was significant for a major depressive episode with suicidal ideation in 1994, 3 years prior to developing PD. Paroxetine reduced the depression modestly, but major improvement occurred when mirtazapine was later substituted. She had not been depressed at the time of the surgery, and family history revealed that her daughter also had major depressive episodes. Prior to DBS surgery, the total levodopa equivalent dose was 1250 mg daily, and the unified Parkinson’s disease rating scale (UPDRS) motor scores were 50 and 32 in the practically defined off and on states, respectively, meeting CAPSIT-PD criteria for dopaminergic responsiveness [11]. DBS electrodes were placed in the STN bilaterally on the same day without complications. Intraoperative testing of the electrodes demonstrated a noticeable reduction in the patient’s bradykinesia and rigidity. Post-operative cranial MRI showed proper placement of both stimulators (Fig. 1A). When the stimulators were first turned on 1 week postoperatively (right side, case positive, three negative, 3.5 V,
Fig. 1. Magnetic resonance images showing proper placement of the DBS electrodes in the subthalamic nuclei bilaterally. (A) T2 axial image postimplantation. (B) T2 axial image post-ECT. (C) T2 axial image post-ECT with superimposed atlas. (D) T2 coronal image post-ECT.
90 ms, 130 Hz; left side, two positive, three negative, 3.5 V, 90 ms, 130 Hz), she noticed a mild-to-moderate improvement in rigidity and bradykinesia. However, her mood quickly worsened over the next few weeks, and she developed mood-congruent paranoid delusions and bizarre thinking, such as the belief that her legs were cut off from her body and the fear that electronic remote controls would turn her stimulators off. She became withdrawn and typically stayed in bed all day. Despite increasing stimulation parameters, her motor function declined rapidly, and dopaminergic medications could not be reduced. She complained of decreased energy, poor sleep and appetite, and repeatedly stated that she wanted to die. Venlafaxine (225 mg daily) was added, but she continued to deteriorate, neglecting basic grooming and hygiene. Turning off the stimulators for 1 week made no difference in her mood, and subsequent substitutions of quetiapine (100 mg qhs) and nortriptyline (100 mg qhs) for venlafaxine were ineffective. Because of her poor response to medical treatment, a course of ECT was recommended, 8 months after DBS surgery. After informed consent for inpatient ECT was obtained from the patient and her family, she received a total of nine treatments over 3 weeks. Quetiapine 100 mg qhs, nortriptyline 75 mg qd, and pre-operative doses of carbidopa/levodopa were continued during ECT. The stimulators were turned off prior to the first ECT treatment and remained off for the duration of her hospital stay. Electrodes were placed bilaterally over the frontal regions as far away from the DBS hardware as possible. Etomidate, 8 mg (used because methohexital was unavailable), was given for anesthesia and succinylcholine, 80 mg, was administered for muscle relaxation prior to each treatment. A Thymatron ECT device (Somatics Inc., Lake Bluff, IL, USA) was used to deliver the treatments, beginning at 45% of maximum charge (pulse widthZ1.0 s, frequencyZ60 sK1, durationZ2.0 s, currentZ0.8 A) for the first session and ending at 75% (pulse widthZ1.4 s, frequencyZ90 sK1, durationZ2.0 s, currentZ0.8 A) for the final treatment. Seizure durations ranged from 21 to 48 s, and the last four treatments were augmented with caffeine to maintain adequate seizure duration. The patient tolerated these treatments well, with only transient confusion after each ECT delivery. After the fourth treatment, the patient became much less fearful, displayed a brighter affect, and demonstrated no delusional thinking. By the end of the seventh treatment, she slept and ate better, and began to comb her hair and brush her teeth independently. At the end of the course of ECT, she was joking and playing checkers with her peers. It was not clear if the patient’s increased animation and physical activity was partly due to the anti-parkinsonian effects of ECT or simply the resolution of psychomotor changes that were a component of her severe depression. Psychotropic medications on discharge were nortriptyline 75 mg qhs and quetiapine 100 mg qhs. Due to logistical issues, it was impractical for the patient to receive maintenance ECT, so she was maintained on her
K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
discharge psychiatric medications post-hospitalization. Post-ECT cranial MRI revealed no shift in electrode position (Fig. 1B–D), and both stimulators were turned on a few weeks after ECT, with noticeable improvement in her motor symptoms. At her last follow-up, approximately 6 months after the ECT treatment, there was no return in depressive or psychotic symptoms. She had no tremor, dyskinesias or fluctuations with monopolar stimulation at settings of 2.2 V, 90 ms, and 130 Hz on the right and 2.3 V, 90 ms, and 185 Hz on the left, which were lower than her stimulation parameters prior to ECT. Her UPDRS motor score was 42, and she was taking a levodopa equivalent dose of 780 mg daily, compared to 1250 mg prior to surgery.
3. Discussion This case demonstrates that ECT can be a safe and effective treatment for severe depression in PD patients who have undergone DBS surgery. ECT is commonly recommended for patients with severe depression who have failed multiple medications [12], but there is minimal clinical experience with this treatment modality following DBS. To our knowledge, this is the first report of ECT in a patient with bilateral STN deep brain stimulators placed for PD. Moscarillo and Annunziata [10] recently reported a single case in which ECT improved depressive symptoms in a patient with DBS. However, their patient had an electrode implanted unilaterally into the thalamus for essential tremor (ET). In bilateral ECT, a seizure is induced by an electrical charge given through scalp electrodes placed in the bitemporal or bifrontal regions. The main concern in delivering ECT to patients with DBS systems is that the electrical charge could induce a radiofrequency current in the DBS electrodes, thus heating them and causing permanent damage to the surrounding brain tissue, similar to what has been reported after diathermy [13] and cardioversion [14]. We believed this risk to be small in our case because the energy needed to induce a seizure is far less than what is traditionally used for cardioversion [15]. Furthermore, we tried to minimize this possibility by placing the ECT electrodes as far away from the DBS hardware as possible. Another concern is that the motor activity induced by the seizure could potentially shift the position of the DBS electrode. Our patient had no shift in electrode position on a post-ECT cranial MRI, and she had an excellent response to DBS after her ECT treatments, suggesting that there was no damage to the electrode(s), pulse generator, or surrounding tissue. An important aspect of this case is the possibility that either the surgical procedure or stimulation of the STN caused the episode of psychotic depression. Severe depression after bilateral STN stimulation for PD has been reported before [4,5,7,8], but the etiology remains unclear. Spread of stimulation to the substantia nigra has been
405
implicated in depression after DBS surgery [3], but our patient’s depression did not improve after discontinuing stimulation prior to ECT treatment and there was no recurrence of her depression when restarting stimulation after ECT. A depressed mood secondary to dopaminergic withdrawal also seems unlikely, since we could not reduce medications until after treatment with ECT. Depression could potentially occur because the surgery failed to improve parkinsonian symptoms, yet the presence of postoperative depression despite clinical motor improvement in our patient and others reported in the literature [4,5,8] argues against this possibility. Houeto et al. [5] reported severe depression after STN DBS surgery in five PD patients, four of whom had a previous history of depressive episodes. Thus, it is possible that personal susceptibility to a mood disorder led to the recurrence of depression in our patient. However, other factors, such as interruption of subcortical mood fibers from surgical placement of the electrodes, may also be responsible. Regardless of the underlying etiology, severe depression after DBS surgery for PD is not uncommon. PD patients undergoing STN stimulation, especially those with a history of major depressive episodes, should be evaluated and followed closely for depression and treated pharmacologically at the first sign of mood deterioration. However, if the depression is severe or refractory to aggressive antidepressant pharmacotherapy, ECT may be a safe and effective option.
References [1] Krack P, Limousin P, Benabid AL, Pollak P. Chronic stimulation of subthalamic nucleus improves levodopa-induced dyskinesias in Parkinson’s disease. Lancet 1997;350(9092):1676. [2] Jaggi JL, Umemura A, Hurtig HI, Siderowf AD, Colcher A, Stern MB, Baltuch GH. Bilateral stimulation of the subthalamic nucleus in Parkinson’s disease: surgical efficacy and prediction of outcome. Stereotact Funct Neurosurg 2004;82(2):104–14. [3] Bejjani BP, Damier P, Arnulf I, Thivard L, Bonnet AM, Dormont D, Cornu P, Pidoux B, Samson Y, Agid Y. Transient acute depression induced by high-frequency deep-brain stimulation. N Engl J Med 1999;340(19):1476–80. [4] Berney A, Vingerhoets F, Perrin A, Guex P, Villemure JG, Burkhard PR, Benkelfat C, Ghika J. Effect on mood of subthalamic DBS for Parkinson’s disease: a consecutive series of 24 patients. Neurology 2002;59(9):1427–9. [5] Houeto JL, Mesnage V, Mallet L, Pillon B, Gargiulo M, du Moncel ST, Bonnet AM, Pidoux B, Dormont D, Cornu P, Agid Y. Behavioural disorders, Parkinson’s disease and subthalamic stimulation. J Neurol Neurosurg Psychiatry 2002;72(6):701–7. [6] Herzog J, Volkmann J, Krack P, Kopper F, Potter M, Lorenz D, Steinbach M, Klebe S, Hamel W, Schrader B, Weinert D, Muller D, Mehdorn HM, Deuschl G. Two-year follow-up of subthalamic deep brain stimulation in Parkinson’s disease. Mov Disord 2003;18(11): 1332–7. [7] Thobois S, Mertens P, Guenot M, Hermier M, Mollion H, Bouvard M, Chazot G, Broussolle E, Sindou M. Subthalamic nucleus stimulation in Parkinson’s disease: clinical evaluation of 18 patients. J Neurol 2002;249(5):529–34.
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K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
[8] Doshi PK, Chhaya N, Bhatt MH. Depression leading to attempted suicide after bilateral subthalamic nucleus stimulation for Parkinson’s disease. Mov Disord 2002;17(5):1084–5. [9] Stern MB. Electroconvulsive therapy in untreated Parkinson’s disease. Mov Disord 1991;6(3):265. [10] Moscarillo FM, Annunziata CM. ECT in a patient with a deep brainstimulating electrode in place. J ECT 2000;16(3):287–90. [11] Defer GL, Widner H, Marie RM, Remy P, Levivier M. Core assessment program for surgical interventional therapies in Parkinson’s disease (CAPSIT-PD). Mov Disord 1999;14(4):572–84.
[12] Thase ME. Treatment of severe depression. J Clin Psychiatry 2000; 61(1):17–25. [13] Nutt JG, Anderson VC, Peacock JH, Hammerstad JP, Burchiel KJ. DBS and diathermy interaction induces severe CNS damage. Neurology 2001;56(10):1384–6. [14] Yamamoto T, Katayama Y, Fukaya C, Kurihara J, Oshima H, Kasai M. Thalamotomy caused by cardioversion in a patient treated with deep brain stimulation. Stereotact Funct Neurosurg 2000;74(2):73–82. [15] Abrams R. Electroconvulsive therapy. 4th ed. New York: Oxford University Press; 2002.
Short communication
Electroconvulsive therapy for depression in a Parkinson’s disease patient with bilateral subthalamic nucleus deep brain stimulators Kelvin L. Choua,*, Howard I. Hurtigb, Jurg L. Jaggib, Gordon H. Baltuchc, Rodney J. Pelchatd, Daniel Weintraubb,e a Department of Clinical Neurosciences, Brown University Medical School, Providence, RI, USA Parkinson’s Disease and Movement Disorders Center, Pennsylvania Hospital, University of Pennsylvania, Philadelphia, PA, USA c Department of Neurosurgery, Penn Neurologic Institute at Pennsylvania Hospital, University of Pennsylvania, Philadelphia, PA, USA d Department of Psychiatry, Jefferson Medical College, Philadelphia, PA, USA e Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA b
Received 4 February 2005; revised 5 April 2005; accepted 6 April 2005
Abstract We report a patient with advanced Parkinson’s disease (PD) who developed a recurrence of major depression with psychotic features after bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) surgery. Electroconvulsive therapy (ECT) dramatically improved the depression without shifting electrode position or damaging the DBS hardware. This case suggests that ECT can be a safe and effective option for severe depression in PD patients treated with STN DBS. q 2005 Elsevier Ltd. All rights reserved. Keywords: Parkinson’s disease; Deep brain stimulation; Subthalamic nucleus; Depression; Electroconvulsive therapy
1. Introduction Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective option for patients with advanced Parkinson’s disease (PD). STN DBS improves motor function, decreases dyskinesias, and reduces levels of dopaminergic medications [1,2]. However, several studies have suggested that STN stimulation can be associated with deleterious effects on mood, especially depression [3–7]. In many cases, depressive symptoms occur within a month post-operatively and resolve either without specific therapy or with minor stimulator adjustments [3,6,7], but depression after DBS surgery can occasionally be refractory to medical management and even result in suicide [5,7,8]. Electroconvulsive therapy (ECT) can be effective for treatment-resistant depression, even in patients with PD [9]. * Corresponding author. Address: Division of Neurology, Memorial Hospital of Rhode Island, 111 Brewster Street, Pawtucket, RI 02860, USA. Tel.: C1 401 729 3757; fax: C1 401 729 3101. E-mail address: [email protected] (K.L. Chou).
1353-8020/$ - see front matter q 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.parkreldis.2005.04.005
However, there is minimal experience with ECT in patients who have undergone DBS procedures [10]. We report a PD patient who developed a recurrence of a major depressive episode with psychotic features after implantation of bilateral STN DBS electrodes and was subsequently treated safely and successfully with ECT.
2. Case report This 66-year-old Greek woman presented with bradykinesia and tremor of the right arm in 1997 at the age of 59. She was diagnosed with PD and started on carbidopa/levodopa with significant benefit. However, classic motor fluctuations developed within 3 years, and dyskinesias became severely disabling. The addition of ropinirole (9 mg daily) and amantadine hydrochloride (200 mg daily) did not ameliorate fluctuations or dyskinesias. Levodopa, when optimally effective (in the ‘on’ state) , allowed her to be independent in all activities of daily living and to walk without an assistive device. During the wearing-off state, she experienced considerable bradykinesia and rigidity, and was unable to walk. Formal
404
K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
neuropsychological testing was not performed due to severe language barriers, but cognitive functioning had remained relatively unimpaired according to the family. She was considered a good candidate for surgery because of the prospect that the marked fluctuations and prolonged off-time would improve significantly. The past medical history was significant for a major depressive episode with suicidal ideation in 1994, 3 years prior to developing PD. Paroxetine reduced the depression modestly, but major improvement occurred when mirtazapine was later substituted. She had not been depressed at the time of the surgery, and family history revealed that her daughter also had major depressive episodes. Prior to DBS surgery, the total levodopa equivalent dose was 1250 mg daily, and the unified Parkinson’s disease rating scale (UPDRS) motor scores were 50 and 32 in the practically defined off and on states, respectively, meeting CAPSIT-PD criteria for dopaminergic responsiveness [11]. DBS electrodes were placed in the STN bilaterally on the same day without complications. Intraoperative testing of the electrodes demonstrated a noticeable reduction in the patient’s bradykinesia and rigidity. Post-operative cranial MRI showed proper placement of both stimulators (Fig. 1A). When the stimulators were first turned on 1 week postoperatively (right side, case positive, three negative, 3.5 V,
Fig. 1. Magnetic resonance images showing proper placement of the DBS electrodes in the subthalamic nuclei bilaterally. (A) T2 axial image postimplantation. (B) T2 axial image post-ECT. (C) T2 axial image post-ECT with superimposed atlas. (D) T2 coronal image post-ECT.
90 ms, 130 Hz; left side, two positive, three negative, 3.5 V, 90 ms, 130 Hz), she noticed a mild-to-moderate improvement in rigidity and bradykinesia. However, her mood quickly worsened over the next few weeks, and she developed mood-congruent paranoid delusions and bizarre thinking, such as the belief that her legs were cut off from her body and the fear that electronic remote controls would turn her stimulators off. She became withdrawn and typically stayed in bed all day. Despite increasing stimulation parameters, her motor function declined rapidly, and dopaminergic medications could not be reduced. She complained of decreased energy, poor sleep and appetite, and repeatedly stated that she wanted to die. Venlafaxine (225 mg daily) was added, but she continued to deteriorate, neglecting basic grooming and hygiene. Turning off the stimulators for 1 week made no difference in her mood, and subsequent substitutions of quetiapine (100 mg qhs) and nortriptyline (100 mg qhs) for venlafaxine were ineffective. Because of her poor response to medical treatment, a course of ECT was recommended, 8 months after DBS surgery. After informed consent for inpatient ECT was obtained from the patient and her family, she received a total of nine treatments over 3 weeks. Quetiapine 100 mg qhs, nortriptyline 75 mg qd, and pre-operative doses of carbidopa/levodopa were continued during ECT. The stimulators were turned off prior to the first ECT treatment and remained off for the duration of her hospital stay. Electrodes were placed bilaterally over the frontal regions as far away from the DBS hardware as possible. Etomidate, 8 mg (used because methohexital was unavailable), was given for anesthesia and succinylcholine, 80 mg, was administered for muscle relaxation prior to each treatment. A Thymatron ECT device (Somatics Inc., Lake Bluff, IL, USA) was used to deliver the treatments, beginning at 45% of maximum charge (pulse widthZ1.0 s, frequencyZ60 sK1, durationZ2.0 s, currentZ0.8 A) for the first session and ending at 75% (pulse widthZ1.4 s, frequencyZ90 sK1, durationZ2.0 s, currentZ0.8 A) for the final treatment. Seizure durations ranged from 21 to 48 s, and the last four treatments were augmented with caffeine to maintain adequate seizure duration. The patient tolerated these treatments well, with only transient confusion after each ECT delivery. After the fourth treatment, the patient became much less fearful, displayed a brighter affect, and demonstrated no delusional thinking. By the end of the seventh treatment, she slept and ate better, and began to comb her hair and brush her teeth independently. At the end of the course of ECT, she was joking and playing checkers with her peers. It was not clear if the patient’s increased animation and physical activity was partly due to the anti-parkinsonian effects of ECT or simply the resolution of psychomotor changes that were a component of her severe depression. Psychotropic medications on discharge were nortriptyline 75 mg qhs and quetiapine 100 mg qhs. Due to logistical issues, it was impractical for the patient to receive maintenance ECT, so she was maintained on her
K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
discharge psychiatric medications post-hospitalization. Post-ECT cranial MRI revealed no shift in electrode position (Fig. 1B–D), and both stimulators were turned on a few weeks after ECT, with noticeable improvement in her motor symptoms. At her last follow-up, approximately 6 months after the ECT treatment, there was no return in depressive or psychotic symptoms. She had no tremor, dyskinesias or fluctuations with monopolar stimulation at settings of 2.2 V, 90 ms, and 130 Hz on the right and 2.3 V, 90 ms, and 185 Hz on the left, which were lower than her stimulation parameters prior to ECT. Her UPDRS motor score was 42, and she was taking a levodopa equivalent dose of 780 mg daily, compared to 1250 mg prior to surgery.
3. Discussion This case demonstrates that ECT can be a safe and effective treatment for severe depression in PD patients who have undergone DBS surgery. ECT is commonly recommended for patients with severe depression who have failed multiple medications [12], but there is minimal clinical experience with this treatment modality following DBS. To our knowledge, this is the first report of ECT in a patient with bilateral STN deep brain stimulators placed for PD. Moscarillo and Annunziata [10] recently reported a single case in which ECT improved depressive symptoms in a patient with DBS. However, their patient had an electrode implanted unilaterally into the thalamus for essential tremor (ET). In bilateral ECT, a seizure is induced by an electrical charge given through scalp electrodes placed in the bitemporal or bifrontal regions. The main concern in delivering ECT to patients with DBS systems is that the electrical charge could induce a radiofrequency current in the DBS electrodes, thus heating them and causing permanent damage to the surrounding brain tissue, similar to what has been reported after diathermy [13] and cardioversion [14]. We believed this risk to be small in our case because the energy needed to induce a seizure is far less than what is traditionally used for cardioversion [15]. Furthermore, we tried to minimize this possibility by placing the ECT electrodes as far away from the DBS hardware as possible. Another concern is that the motor activity induced by the seizure could potentially shift the position of the DBS electrode. Our patient had no shift in electrode position on a post-ECT cranial MRI, and she had an excellent response to DBS after her ECT treatments, suggesting that there was no damage to the electrode(s), pulse generator, or surrounding tissue. An important aspect of this case is the possibility that either the surgical procedure or stimulation of the STN caused the episode of psychotic depression. Severe depression after bilateral STN stimulation for PD has been reported before [4,5,7,8], but the etiology remains unclear. Spread of stimulation to the substantia nigra has been
405
implicated in depression after DBS surgery [3], but our patient’s depression did not improve after discontinuing stimulation prior to ECT treatment and there was no recurrence of her depression when restarting stimulation after ECT. A depressed mood secondary to dopaminergic withdrawal also seems unlikely, since we could not reduce medications until after treatment with ECT. Depression could potentially occur because the surgery failed to improve parkinsonian symptoms, yet the presence of postoperative depression despite clinical motor improvement in our patient and others reported in the literature [4,5,8] argues against this possibility. Houeto et al. [5] reported severe depression after STN DBS surgery in five PD patients, four of whom had a previous history of depressive episodes. Thus, it is possible that personal susceptibility to a mood disorder led to the recurrence of depression in our patient. However, other factors, such as interruption of subcortical mood fibers from surgical placement of the electrodes, may also be responsible. Regardless of the underlying etiology, severe depression after DBS surgery for PD is not uncommon. PD patients undergoing STN stimulation, especially those with a history of major depressive episodes, should be evaluated and followed closely for depression and treated pharmacologically at the first sign of mood deterioration. However, if the depression is severe or refractory to aggressive antidepressant pharmacotherapy, ECT may be a safe and effective option.
References [1] Krack P, Limousin P, Benabid AL, Pollak P. Chronic stimulation of subthalamic nucleus improves levodopa-induced dyskinesias in Parkinson’s disease. Lancet 1997;350(9092):1676. [2] Jaggi JL, Umemura A, Hurtig HI, Siderowf AD, Colcher A, Stern MB, Baltuch GH. Bilateral stimulation of the subthalamic nucleus in Parkinson’s disease: surgical efficacy and prediction of outcome. Stereotact Funct Neurosurg 2004;82(2):104–14. [3] Bejjani BP, Damier P, Arnulf I, Thivard L, Bonnet AM, Dormont D, Cornu P, Pidoux B, Samson Y, Agid Y. Transient acute depression induced by high-frequency deep-brain stimulation. N Engl J Med 1999;340(19):1476–80. [4] Berney A, Vingerhoets F, Perrin A, Guex P, Villemure JG, Burkhard PR, Benkelfat C, Ghika J. Effect on mood of subthalamic DBS for Parkinson’s disease: a consecutive series of 24 patients. Neurology 2002;59(9):1427–9. [5] Houeto JL, Mesnage V, Mallet L, Pillon B, Gargiulo M, du Moncel ST, Bonnet AM, Pidoux B, Dormont D, Cornu P, Agid Y. Behavioural disorders, Parkinson’s disease and subthalamic stimulation. J Neurol Neurosurg Psychiatry 2002;72(6):701–7. [6] Herzog J, Volkmann J, Krack P, Kopper F, Potter M, Lorenz D, Steinbach M, Klebe S, Hamel W, Schrader B, Weinert D, Muller D, Mehdorn HM, Deuschl G. Two-year follow-up of subthalamic deep brain stimulation in Parkinson’s disease. Mov Disord 2003;18(11): 1332–7. [7] Thobois S, Mertens P, Guenot M, Hermier M, Mollion H, Bouvard M, Chazot G, Broussolle E, Sindou M. Subthalamic nucleus stimulation in Parkinson’s disease: clinical evaluation of 18 patients. J Neurol 2002;249(5):529–34.
406
K.L. Chou et al. / Parkinsonism and Related Disorders 11 (2005) 403–406
[8] Doshi PK, Chhaya N, Bhatt MH. Depression leading to attempted suicide after bilateral subthalamic nucleus stimulation for Parkinson’s disease. Mov Disord 2002;17(5):1084–5. [9] Stern MB. Electroconvulsive therapy in untreated Parkinson’s disease. Mov Disord 1991;6(3):265. [10] Moscarillo FM, Annunziata CM. ECT in a patient with a deep brainstimulating electrode in place. J ECT 2000;16(3):287–90. [11] Defer GL, Widner H, Marie RM, Remy P, Levivier M. Core assessment program for surgical interventional therapies in Parkinson’s disease (CAPSIT-PD). Mov Disord 1999;14(4):572–84.
[12] Thase ME. Treatment of severe depression. J Clin Psychiatry 2000; 61(1):17–25. [13] Nutt JG, Anderson VC, Peacock JH, Hammerstad JP, Burchiel KJ. DBS and diathermy interaction induces severe CNS damage. Neurology 2001;56(10):1384–6. [14] Yamamoto T, Katayama Y, Fukaya C, Kurihara J, Oshima H, Kasai M. Thalamotomy caused by cardioversion in a patient treated with deep brain stimulation. Stereotact Funct Neurosurg 2000;74(2):73–82. [15] Abrams R. Electroconvulsive therapy. 4th ed. New York: Oxford University Press; 2002.