Official journal of the Pacific Rim College of Psychiatrists
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Asia-Pacific Psychiatry ISSN 1758-5864
CLINICAL CASE CONFERENCE
Electroconvulsive therapy for major depressive disorder in a patient with a permanent skull defect: A case report Jihyun Roh MD, Min-Hee Kang MD PhD, Chul-Eung Kim MD PhD, Jeong-Seop Lee MD PhD & Jae-Nam Bae MD PhD Department of Psychiatry, Inha University Hospital, Incheon, Korea
Keywords ECT, MDD, skull defect Correspondence Jae-Nam Bae MD PhD, Department of Psychiatry, College of Medicine, Inha University, 7–206, 3-ga Sinheung Dong, Jung-Gu, Incheon, 400-711, Republic of Korea. Tel: +82 328 903 592 Fax: +82 328 903 559 Email: [email protected]
Abstract Electroconvulsive therapy (ECT) is an effective and safe treatment method for a variety of psychiatric disorders, including major depressive disorder. Although there is no absolute contraindication to ECT, clinicians often hesitate to apply this method to patients with a skull defect. We report a case of ECT performed on a major depressive disorder patient with an open wound after craniectomy. We summarize successful ECT cases of patients with a permanent skull defect and discuss various factors that may influence ECT outcomes in patients with a skull defect, including electrode placement, benzodiazepines, and anticonvulsants.
Received 21 December 2013 Accepted 4 March 2014 DOI:10.1111/appy.12130
Introduction Electroconvulsive therapy (ECT) is an effective and safe treatment method for a variety of psychiatric disorders, including major depressive disorder (MDD) (Kelly and Zisselman, 2000). In the case of patients with a skull defect, however, clinicians often hesitate to apply this method because of a lack of related case reports. Although there is no absolute contraindication to ECT (American Psychiatric Association, 2001), according to a previous study, the potential risk of brain damage could be increased when the patient has a craniotomy opening or a congenital defect in the skull (Gordon, 1982). This suggests that patients with a skull defect are more vulnerable to the risk of prolonged seizures or cognitive side-effects when ECT is applied. Therefore, some procedures require considerable attention prior to ECT use. We report a case of ECT for a man with a permanent skull defect who suffered from severe depression.
Case report A 64-year-old man was admitted to a psychiatric unit with complaints of anxiety, insomnia, and suicidal
454
ideation. His agitation and depression worsened over a seven-month period, exhibiting an obsession with suicide. He also experienced weight loss of 8 kg. Initial severity of depression was scored at 33 on the Hamilton Depression Rating Scale (HAM-D) (Hamilton, 1960), and suicidality reached 24 on the Beck’s Scale for Suicidal Ideation (SSI) (Beck et al., 1979). He had a similar history of agitated depression 20 years ago, which led him to attempt suicide by jumping off a rock. He was admitted to a neurosurgery department for 4 months and underwent decompressive craniectomy. After surgery, he reported no changes in his personality, cognitive impairment, convulsion, or other neurologic symptoms. At the time of this hospitalization, his skull X-ray showed a 5 × 6 cm skull defect on the left parietal vertex and a 0.5 × 2 × 0.5 cm skull dent at the center of the forehead (Figure 1). His brain computed tomography (CT) showed mild encephalomalacia near the parietal vertex. He took his medication, including anxiolytics, for a month before hospitalization but did not perceive any changes in his symptoms. We increased his daily oral medication dose to duloxetine 90 mg, aripiprazole 10 mg, alprazolam 0.75 mg, and buspirone 15 mg. However, he remained pessimistic and lethargic,
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
J. Roh et al.
ECT for MDD in a patient with a skull defect
Figure 1. The skull X-ray of the patient (A 5 × 6 cm skull defect is on the left parietal vertex).
complaining of severe dyspepsia. In addition, he still clearly showed suicidal tendencies. Because of the high suicide risk, we started modified ECT three times a week, for a total of nine treatments starting on the 19th day of hospitalization. We did not reduce the dose of alprazolam in preparation because of the relatively high risk of seizures and maintained other medications because of the severity of symptoms. We consulted with the neurology department prior to ECT to take immediate action in case of status epilepticus. In addition, 4 mg of IV lorazepam was prepared in advance. Propofol 120 mg, glycopyrrolate 0.2 mg, and succinylcholine 60 mg were used as anesthetics. Brief pulse stimulation with the MECTA SR-1 machine was used. To reduce the risk of an irreversible change in brain tissue (Gordon, 1982), electrodes were bifrontally placed, avoiding the skull dent at the center of the forehead, at nearly equal distances from the skull defect (Figure 2). The minimum stimulation to induce a seizure was 31.6 J (1.0 ms pulse width, 70 Hz frequency, 2.0-second duration, 800 mA current), and the seizure time was up to 55 seconds. From the day of the first ECT, the patient completed almost every meal, and his complaints about dyspepsia were significantly reduced. After three treatments, he felt more comfortable and satisfied with his sleep. By the sixth treatment, he participated voluntarily in a group therapy session and started to make plans for his life after discharge. Following the ninth treatment, he was discharged with significant improvements. Upon discharge, his HAM-D and SSI scores decreased to 11 and 0, respectively. During the ECT period, postictal confusion occurred once (after
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
Figure 2. The electrode placement (electrodes were bifrontally placed at nearly equal distances from the skull defect on the left parietal vertex to avoid the skull dent at the center of the forehead).
the eighth treatment) but completely disappeared within an hour. No neurologic or cognitive signs were encountered during the entire hospitalization period. During the 3-month follow-up visit, he was functioning well in daily living, without any complaints of anxiety.
Discussion This clinical report demonstrates the effectiveness and safety of ECT for MDD in a patient with a permanent skull defect. The patient received ECT a total of nine treatments and showed definite improvements without significant adverse effects. In general, conditions that increase intracranial pressure are known to be relative contraindications to ECT(American Psychiatric Association, 2001). The effects of a skull defect or a history of open brain surgery remain unclear. There are several cases of ECT after craniotomy (Ruedrich et al., 1983; Hsiao and Evans, 1984; Levy and Levy, 1987; Hartmann and
455
456
None 9 2 1.0 70 800mA Bifrontal None Lt parietal 64 Roh et al. (2014)
M
16 Ghaziuddin et al. (1999)
This table was modified based on the table in Amanullah et al. (2012). ECT, electroconvulsive therapy; MDD, major depressive disorder; NR, not referenced; VP, Ventriculoperitoneal.
MECTA SR-1
67 Everman et al. (1999)
F
Suboccipital
VP shunt
Manic episode MDD
MECTA SR-1
None 12 NR NR NR NR
None 9 NR NR NR THYMATRON DGx MDD NR Rt temporal
79 Everman et al. (1999)
F
Lt temporal
59
M
Rt frontoparietal
50–100%
Confusion 7 NR NR MDD
THYMATRON DGx
Modified bilateral Modified Rt unilateral Bilateral
10–50%
NR
None 12 1.25 1.6 80 700mA Bilateral MECTA SR-1 MDD
None 17 0.75 1.2 30 NR Bitemporal
Hartmann et al. (1990)
M
ECT machine
NR MDD
Diagnosis Other brain lesions
Bone and metallic fragments Shrapnel in zygoma NR Rt parietal
Skull defect
21
Gender Age Author
Ruedrich et al. (1983)
F
Total ECT Duration (seconds) Pulse width (ms) Frequency (Hz) Current/ energy level Electrode placement Table 1. Successful ECT cases of patients with skull defects
Saldivia, 1990; Starkstein and Migliorelli, 1993; Everman et al., 1999; Ghaziuddin et al., 1999; Gursky et al., 2000; Madan and Anderson, 2001; Amanullah et al., 2012), but these reports show heterogeneity when it comes to craniotomy and the type of skull defect. As shown in Table 1, fewer cases of patients undergoing ECT with a permanent skull defect, as shown in the present case, have been reported (Ruedrich et al., 1983; Hartmann and Saldivia, 1990; Everman et al., 1999; Ghaziuddin et al., 1999). There are two cases of ECT after craniectomy (Hartmann and Saldivia, 1990; Ghaziuddin et al., 1999). Out of these cases with permanent skull defects only one (Everman et al., 1999) reported severe confusion near the end of the treatment, which cleared within 10 days. The others reported no other neurologic or cognitive symptoms. According to a previous cadaver experiment (Gordon, 1982), all electricity entering the skull when one electrode is near a congenital defect or a craniotomy opening is concentrated in a relatively small part of the cortex immediately below the defect. This greatly increases the risk of an irreversible change in brain tissue. In such cases, therefore, electrodes must be placed at approximately equal distances from the defect. We placed electrodes bifrontally to avoid the defect and found no sign suggesting any brain injury. The seizure threshold and duration in this case are not significantly different from those in other cases without skull defects. First, it may be due to preventing lowering of seizure threshold by using bifrontal electrode placement (Sackeim et al., 1987; Bailine et al., 2000; Kellner et al., 2010). Second, maintaining doses of benzodiazepines can also contribute to this result. According to Hsiao and Evans (1984), they used phenobarbital during ECT period for a patient with postcraniectomy seizures. There is another case of phenobarbital prophylaxis for post-ECT seizures (Ruedrich et al., 1983). In sum, ECT can be an effective and safe method for MDD patients with a permanent skull defect after craniectomy. It is vital to adjust the electrode placement to prevent the patients from receiving brain damage from a skull defect. The dosage of combination drugs, which affects the seizure threshold or clinical symptoms, should also be emphasized. Drugs such as benzodiazepines are routinely reduced before ECT, but they can be maintained when necessary. We did not trial prophylactic classical anticonvulsants in this case. However, some other cases suggest its protective effect, therefore it merits further attention.
J. Roh et al.
Serious adverse event
ECT for MDD in a patient with a skull defect
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
J. Roh et al.
References Amanullah S., Delva N., McRae H., Campbell L.A., Cole J. (2012) Electroconvulsive therapy in patients with skull defects or metallic implants: a review of the literature and case report. Prim Care Companion CNS Disord. 14. doi: 10.4088/PCC.11r01228 American Psychiatric Association (2001) The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging, 2nd edn. American Psychiatric Association, Washington, DC.
ECT for MDD in a patient with a skull defect
Hartmann S.J., Saldivia A. (1990) ECT in an elderly patient with skull defects and shrapnel. Convuls Ther. 6, 165–171. Hsiao J.K., Evans D.L. (1984) ECT in a depressed patient after craniotomy. Am J Psychiatry. 141, 442–444. Kellner C.H., Knapp R., Husain M.M., et al. (2010) Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. Br J Psychiatry. 196, 226–234.
Bailine S.H., Rifkin A., Kayne E., et al. (2000) Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry. 157, 121–123.
Kelly K.G., Zisselman M. (2000) Update on electroconvulsive therapy (ECT) in older adults. J Am Geriatr Soc. 48, 560–566.
Beck A.T., Kovacs M., Weissman A. (1979) Assessment of suicidal intention: the Scale for Suicide Ideation. J Consult Clin Psychol. 47, 343–352.
Levy S.D., Levy S.B. (1987) Electroconvulsive therapy in two former neurosurgical patients: skull prosthesis and ventricular shunt. Convuls Ther. 3, 46–48.
Everman P.D. Jr, Kellner C.H., Beale M.D., Burns C. (1999) Modified electrode placement in patients with neurosurgical skull defects. J ECT. 15, 237–239.
Madan S., Anderson K. (2001) ECT for a patient with a metallic skull plate. J ECT. 17, 289–291.
Ghaziuddin N., DeQuardo J.R., Ghaziuddin M., King C.A. (1999) Electroconvulsive treatment of a bipolar adolescent postcraniotomy for brain stem astrocytoma. J Child Adolesc Psychopharmacol. 9, 63–69. Gordon D. (1982) Electro-convulsive therapy with minimum hazard. Br J Psychiatry. 141, 12–18. Gursky J.T., Rummans T.A., Black J.L. (2000) ECT administration in a patient after craniotomy and gamma knife surgery: a case report and review. J ECT. 16, 295–299. Hamilton M. (1960) A rating scale for depression. J Neurol Neurosurg Psychiatry. 23, 56–62.
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
Roh J., Kang M.-H., Kim C.-E., Lee J.-S., Bae J.-N. (2014) Electroconvulsive therapy for major depressive disorder in a patient with a permanent skull defect: a case report. (in press). Ruedrich S.L., Chu C.C., Moore S.L. (1983) ECT for major depression in a patient with acute brain trauma. Am J Psychiatry. 140, 928–929. Sackeim H., Decina P., Prohovnik I., Malitz S. (1987) Seizure threshold in electroconvulsive therapy. Effects of sex, age, electrode placement, and number of treatments. Arch Gen Psychiatry. 44, 355–360. Starkstein S.E., Migliorelli R. (1993) ECT in a patient with a frontal craniotomy and residual meningioma. J Neuropsychiatry Clin Neurosci. 5, 428–430.
457
Copyright of Asia-Pacific Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
bs_bs_banner
Asia-Pacific Psychiatry ISSN 1758-5864
CLINICAL CASE CONFERENCE
Electroconvulsive therapy for major depressive disorder in a patient with a permanent skull defect: A case report Jihyun Roh MD, Min-Hee Kang MD PhD, Chul-Eung Kim MD PhD, Jeong-Seop Lee MD PhD & Jae-Nam Bae MD PhD Department of Psychiatry, Inha University Hospital, Incheon, Korea
Keywords ECT, MDD, skull defect Correspondence Jae-Nam Bae MD PhD, Department of Psychiatry, College of Medicine, Inha University, 7–206, 3-ga Sinheung Dong, Jung-Gu, Incheon, 400-711, Republic of Korea. Tel: +82 328 903 592 Fax: +82 328 903 559 Email: [email protected]
Abstract Electroconvulsive therapy (ECT) is an effective and safe treatment method for a variety of psychiatric disorders, including major depressive disorder. Although there is no absolute contraindication to ECT, clinicians often hesitate to apply this method to patients with a skull defect. We report a case of ECT performed on a major depressive disorder patient with an open wound after craniectomy. We summarize successful ECT cases of patients with a permanent skull defect and discuss various factors that may influence ECT outcomes in patients with a skull defect, including electrode placement, benzodiazepines, and anticonvulsants.
Received 21 December 2013 Accepted 4 March 2014 DOI:10.1111/appy.12130
Introduction Electroconvulsive therapy (ECT) is an effective and safe treatment method for a variety of psychiatric disorders, including major depressive disorder (MDD) (Kelly and Zisselman, 2000). In the case of patients with a skull defect, however, clinicians often hesitate to apply this method because of a lack of related case reports. Although there is no absolute contraindication to ECT (American Psychiatric Association, 2001), according to a previous study, the potential risk of brain damage could be increased when the patient has a craniotomy opening or a congenital defect in the skull (Gordon, 1982). This suggests that patients with a skull defect are more vulnerable to the risk of prolonged seizures or cognitive side-effects when ECT is applied. Therefore, some procedures require considerable attention prior to ECT use. We report a case of ECT for a man with a permanent skull defect who suffered from severe depression.
Case report A 64-year-old man was admitted to a psychiatric unit with complaints of anxiety, insomnia, and suicidal
454
ideation. His agitation and depression worsened over a seven-month period, exhibiting an obsession with suicide. He also experienced weight loss of 8 kg. Initial severity of depression was scored at 33 on the Hamilton Depression Rating Scale (HAM-D) (Hamilton, 1960), and suicidality reached 24 on the Beck’s Scale for Suicidal Ideation (SSI) (Beck et al., 1979). He had a similar history of agitated depression 20 years ago, which led him to attempt suicide by jumping off a rock. He was admitted to a neurosurgery department for 4 months and underwent decompressive craniectomy. After surgery, he reported no changes in his personality, cognitive impairment, convulsion, or other neurologic symptoms. At the time of this hospitalization, his skull X-ray showed a 5 × 6 cm skull defect on the left parietal vertex and a 0.5 × 2 × 0.5 cm skull dent at the center of the forehead (Figure 1). His brain computed tomography (CT) showed mild encephalomalacia near the parietal vertex. He took his medication, including anxiolytics, for a month before hospitalization but did not perceive any changes in his symptoms. We increased his daily oral medication dose to duloxetine 90 mg, aripiprazole 10 mg, alprazolam 0.75 mg, and buspirone 15 mg. However, he remained pessimistic and lethargic,
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
J. Roh et al.
ECT for MDD in a patient with a skull defect
Figure 1. The skull X-ray of the patient (A 5 × 6 cm skull defect is on the left parietal vertex).
complaining of severe dyspepsia. In addition, he still clearly showed suicidal tendencies. Because of the high suicide risk, we started modified ECT three times a week, for a total of nine treatments starting on the 19th day of hospitalization. We did not reduce the dose of alprazolam in preparation because of the relatively high risk of seizures and maintained other medications because of the severity of symptoms. We consulted with the neurology department prior to ECT to take immediate action in case of status epilepticus. In addition, 4 mg of IV lorazepam was prepared in advance. Propofol 120 mg, glycopyrrolate 0.2 mg, and succinylcholine 60 mg were used as anesthetics. Brief pulse stimulation with the MECTA SR-1 machine was used. To reduce the risk of an irreversible change in brain tissue (Gordon, 1982), electrodes were bifrontally placed, avoiding the skull dent at the center of the forehead, at nearly equal distances from the skull defect (Figure 2). The minimum stimulation to induce a seizure was 31.6 J (1.0 ms pulse width, 70 Hz frequency, 2.0-second duration, 800 mA current), and the seizure time was up to 55 seconds. From the day of the first ECT, the patient completed almost every meal, and his complaints about dyspepsia were significantly reduced. After three treatments, he felt more comfortable and satisfied with his sleep. By the sixth treatment, he participated voluntarily in a group therapy session and started to make plans for his life after discharge. Following the ninth treatment, he was discharged with significant improvements. Upon discharge, his HAM-D and SSI scores decreased to 11 and 0, respectively. During the ECT period, postictal confusion occurred once (after
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
Figure 2. The electrode placement (electrodes were bifrontally placed at nearly equal distances from the skull defect on the left parietal vertex to avoid the skull dent at the center of the forehead).
the eighth treatment) but completely disappeared within an hour. No neurologic or cognitive signs were encountered during the entire hospitalization period. During the 3-month follow-up visit, he was functioning well in daily living, without any complaints of anxiety.
Discussion This clinical report demonstrates the effectiveness and safety of ECT for MDD in a patient with a permanent skull defect. The patient received ECT a total of nine treatments and showed definite improvements without significant adverse effects. In general, conditions that increase intracranial pressure are known to be relative contraindications to ECT(American Psychiatric Association, 2001). The effects of a skull defect or a history of open brain surgery remain unclear. There are several cases of ECT after craniotomy (Ruedrich et al., 1983; Hsiao and Evans, 1984; Levy and Levy, 1987; Hartmann and
455
456
None 9 2 1.0 70 800mA Bifrontal None Lt parietal 64 Roh et al. (2014)
M
16 Ghaziuddin et al. (1999)
This table was modified based on the table in Amanullah et al. (2012). ECT, electroconvulsive therapy; MDD, major depressive disorder; NR, not referenced; VP, Ventriculoperitoneal.
MECTA SR-1
67 Everman et al. (1999)
F
Suboccipital
VP shunt
Manic episode MDD
MECTA SR-1
None 12 NR NR NR NR
None 9 NR NR NR THYMATRON DGx MDD NR Rt temporal
79 Everman et al. (1999)
F
Lt temporal
59
M
Rt frontoparietal
50–100%
Confusion 7 NR NR MDD
THYMATRON DGx
Modified bilateral Modified Rt unilateral Bilateral
10–50%
NR
None 12 1.25 1.6 80 700mA Bilateral MECTA SR-1 MDD
None 17 0.75 1.2 30 NR Bitemporal
Hartmann et al. (1990)
M
ECT machine
NR MDD
Diagnosis Other brain lesions
Bone and metallic fragments Shrapnel in zygoma NR Rt parietal
Skull defect
21
Gender Age Author
Ruedrich et al. (1983)
F
Total ECT Duration (seconds) Pulse width (ms) Frequency (Hz) Current/ energy level Electrode placement Table 1. Successful ECT cases of patients with skull defects
Saldivia, 1990; Starkstein and Migliorelli, 1993; Everman et al., 1999; Ghaziuddin et al., 1999; Gursky et al., 2000; Madan and Anderson, 2001; Amanullah et al., 2012), but these reports show heterogeneity when it comes to craniotomy and the type of skull defect. As shown in Table 1, fewer cases of patients undergoing ECT with a permanent skull defect, as shown in the present case, have been reported (Ruedrich et al., 1983; Hartmann and Saldivia, 1990; Everman et al., 1999; Ghaziuddin et al., 1999). There are two cases of ECT after craniectomy (Hartmann and Saldivia, 1990; Ghaziuddin et al., 1999). Out of these cases with permanent skull defects only one (Everman et al., 1999) reported severe confusion near the end of the treatment, which cleared within 10 days. The others reported no other neurologic or cognitive symptoms. According to a previous cadaver experiment (Gordon, 1982), all electricity entering the skull when one electrode is near a congenital defect or a craniotomy opening is concentrated in a relatively small part of the cortex immediately below the defect. This greatly increases the risk of an irreversible change in brain tissue. In such cases, therefore, electrodes must be placed at approximately equal distances from the defect. We placed electrodes bifrontally to avoid the defect and found no sign suggesting any brain injury. The seizure threshold and duration in this case are not significantly different from those in other cases without skull defects. First, it may be due to preventing lowering of seizure threshold by using bifrontal electrode placement (Sackeim et al., 1987; Bailine et al., 2000; Kellner et al., 2010). Second, maintaining doses of benzodiazepines can also contribute to this result. According to Hsiao and Evans (1984), they used phenobarbital during ECT period for a patient with postcraniectomy seizures. There is another case of phenobarbital prophylaxis for post-ECT seizures (Ruedrich et al., 1983). In sum, ECT can be an effective and safe method for MDD patients with a permanent skull defect after craniectomy. It is vital to adjust the electrode placement to prevent the patients from receiving brain damage from a skull defect. The dosage of combination drugs, which affects the seizure threshold or clinical symptoms, should also be emphasized. Drugs such as benzodiazepines are routinely reduced before ECT, but they can be maintained when necessary. We did not trial prophylactic classical anticonvulsants in this case. However, some other cases suggest its protective effect, therefore it merits further attention.
J. Roh et al.
Serious adverse event
ECT for MDD in a patient with a skull defect
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
J. Roh et al.
References Amanullah S., Delva N., McRae H., Campbell L.A., Cole J. (2012) Electroconvulsive therapy in patients with skull defects or metallic implants: a review of the literature and case report. Prim Care Companion CNS Disord. 14. doi: 10.4088/PCC.11r01228 American Psychiatric Association (2001) The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging, 2nd edn. American Psychiatric Association, Washington, DC.
ECT for MDD in a patient with a skull defect
Hartmann S.J., Saldivia A. (1990) ECT in an elderly patient with skull defects and shrapnel. Convuls Ther. 6, 165–171. Hsiao J.K., Evans D.L. (1984) ECT in a depressed patient after craniotomy. Am J Psychiatry. 141, 442–444. Kellner C.H., Knapp R., Husain M.M., et al. (2010) Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. Br J Psychiatry. 196, 226–234.
Bailine S.H., Rifkin A., Kayne E., et al. (2000) Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry. 157, 121–123.
Kelly K.G., Zisselman M. (2000) Update on electroconvulsive therapy (ECT) in older adults. J Am Geriatr Soc. 48, 560–566.
Beck A.T., Kovacs M., Weissman A. (1979) Assessment of suicidal intention: the Scale for Suicide Ideation. J Consult Clin Psychol. 47, 343–352.
Levy S.D., Levy S.B. (1987) Electroconvulsive therapy in two former neurosurgical patients: skull prosthesis and ventricular shunt. Convuls Ther. 3, 46–48.
Everman P.D. Jr, Kellner C.H., Beale M.D., Burns C. (1999) Modified electrode placement in patients with neurosurgical skull defects. J ECT. 15, 237–239.
Madan S., Anderson K. (2001) ECT for a patient with a metallic skull plate. J ECT. 17, 289–291.
Ghaziuddin N., DeQuardo J.R., Ghaziuddin M., King C.A. (1999) Electroconvulsive treatment of a bipolar adolescent postcraniotomy for brain stem astrocytoma. J Child Adolesc Psychopharmacol. 9, 63–69. Gordon D. (1982) Electro-convulsive therapy with minimum hazard. Br J Psychiatry. 141, 12–18. Gursky J.T., Rummans T.A., Black J.L. (2000) ECT administration in a patient after craniotomy and gamma knife surgery: a case report and review. J ECT. 16, 295–299. Hamilton M. (1960) A rating scale for depression. J Neurol Neurosurg Psychiatry. 23, 56–62.
Asia-Pacific Psychiatry 6 (2014) 454–457 © 2014 Wiley Publishing Asia Pty Ltd
Roh J., Kang M.-H., Kim C.-E., Lee J.-S., Bae J.-N. (2014) Electroconvulsive therapy for major depressive disorder in a patient with a permanent skull defect: a case report. (in press). Ruedrich S.L., Chu C.C., Moore S.L. (1983) ECT for major depression in a patient with acute brain trauma. Am J Psychiatry. 140, 928–929. Sackeim H., Decina P., Prohovnik I., Malitz S. (1987) Seizure threshold in electroconvulsive therapy. Effects of sex, age, electrode placement, and number of treatments. Arch Gen Psychiatry. 44, 355–360. Starkstein S.E., Migliorelli R. (1993) ECT in a patient with a frontal craniotomy and residual meningioma. J Neuropsychiatry Clin Neurosci. 5, 428–430.
457
Copyright of Asia-Pacific Psychiatry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
