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• W4296625101 abstract "Electroconvulsive therapy (ECT) is sometimes used for treatment-resistant depressive symptoms in patients with dementia with Lewy bodies (DLB). It has been thought that the existence of intracranial lesions, including aneurysms, could increase the risk of complications with ECT. Recently, the number of cases of asymptomatic aneurysms, as well as coil embolisation for them, have increased. Given the increasing number of patients with DLB, we believe there will be more opportunities for ECT in patients who have been treated for cerebral aneurysms with coil embolisation. However, to the best of our knowledge, there have been very few case reports regarding ECT in patients with DLB treated with post-coil embolisation. Here, we report a case of ECT performed on a patient with DLB plus depressive symptoms and after post-coil embolisation for a cerebral aneurysm. The patient has provided their written informed consent for the publication of this manuscript (references for this section are available in the Supplementary materials). A 74-year-old Japanese woman was admitted to our hospital after attempted suicide. At 70 years of age, she underwent coil embolisation for an asymptomatic and unruptured anterior communicating aneurysm. The aneurysm was embolised using a target 360 detachable coil and an occlusion balloon catheter. At 72 years of age, her memory function began to decline. At 74 years of age, rapid eye movement (REM) sleep behaviour abnormalities, such as talking in her sleep with motions like paddling a canoe, lasted for 1 h. Furthermore, she experienced constipation, orthostatic dizziness, and loss of smell. Visual hallucinations, for example, policemen appearing at her house or her neighbours cooking in the kitchen, frequently occurred. Parkinsonism with continuous mild rest tremor in her right hand and fluctuating cognition also appeared. In addition, depressed mood, loss of interest, decreased motivation, and delusion of guilt were also observed. Her appetite diminished, and she lost 20 kg within 3 months. Her Mini-Mental State Examination score was 15, and she had moderate cognitive impairment. In terms of brain imaging, the magnetic resonance imaging (MRI) showed age-appropriate brain atrophy, and magnetic resonance angiography demonstrated neither blood flow signal at her coil embolisation site nor any new aneurysm (Fig. 1). Single-photon emission computed tomography (SPECT) showed decreased blood flow in the occipital lobe, and dopamine transporter (DAT) imaging demonstrated decreased DAT in the left dorsal striatum; quantitative assessment by the Specific Binding Ration Bolt-Age Correlation showed the normal DAT availability (lower limit of normal), but a radiologist and we visually judged that the DAT uptake was reduced mildly in the left striatum (Fig. 2). Her score on the 21-item Hamilton Depression Rating Scale (HAM-D) was 37, indicating severe depressive status. Her vital signs including blood pressure, laboratory data, and electrocardiogram findings were within the normal limits. According to the DLB diagnostic criteria, she had declined memory function (dementia), four core clinical features (fluctuating cognition, recurrent visual hallucinations, REM sleep behaviour disorder, and spontaneous features of parkinsonism), one supportive clinical feature (depressive symptoms), and two supportive biomarkers (relative preservation of medial temporal lobe structures on the MRI scan, and generalised low uptake on the SPECT perfusion scan with reduced occipital activity), we diagnosed her with probable DLB with severe depressive symptoms. Treatment with antidepressants (mirtazapine, vortioxetine, and duloxetine), donepezil, and olanzapine was initiated (we had obtained consent from the patient and her family for the use of olanzapine); however, her depressive symptoms remained severe. Specifically, vortioxetine (20 mg/day for 4 weeks) and duloxetine (60 mg/day for 4 weeks) were not effective on her depressive symptoms. Then, we started to replace duloxetine with mirtazapine. However, her depressive symptoms got worse when mirtazapine was administered at 30 mg/day. We therefore judged her symptoms as treatment-resistant, and thought that ECT was necessary. An anaesthesiologist and neurosurgeon were consulted regarding the safety of ECT for her. The patient and her family provided informed consent and agreed to our treatment plan. The ECT was conducted using Thymatron (Somatics Inc., Lake Bluff, IL, USA) with a bitemporal arrangement of electrodes. She received six sessions of ECT with stimulus intensity ranging from 35% to 100%. General anaesthesia was induced by an anaesthesiologist using propofol (1.0 mg/kg), and muscular paralysis was induced using succinylcholine (1.0 mg/kg). Her systolic blood pressure was maintained at 190 mmHg, and her heart rate was maintained at <100 bpm. Her baseline blood pressure was 110/60 mmHg, and her heart rate was 60 bpm. We did not use any drugs to maintain her blood pressure and heart rate during ECT or at any other time. Her depressive symptoms gradually improved, and she was able to eat after the fourth session of ECT. After the sixth session, the improvement in her depressive symptoms appeared to have reached a plateau and ECT was terminated. Her HAM-D score improved to five, and visual hallucinations and sleep-talking disappeared. We performed ECT for severe depressive symptoms in a patient with DLB who underwent post-coil embolisation of a cerebral aneurysm. The treatment was completed without any serious adverse events. A previous report demonstrated the efficacy of ECT for treatment-resistant depressive symptoms in patients with DLB. Takahashi et al. (2009) reported that ECT was conducted for severe depressive symptoms in three patients with probable DLB and five with possible DLB, and all of their HAM-D scores were improved (mean score ± SD: 38.0 ± 5.8 before ECT; 15.0 ± 9.6 after ECT) (1). In terms of ECT for post-coil embolisation, Van Herck et al. (2009) summarised 15 cases of ECT with untreated or post-treated cerebral aneurysms (2). They reported that two cases had post-coil embolisation and showed no major complications with ECT. There have been some previous studies on aneurysm dynamics after coil embolisation. Reul et al. (1998) performed a pathological analysis on rabbits to evaluate biological changes 3 weeks after coil embolisation (3). Specifically, they artificially created terminal artery bifurcation aneurysms in rabbits. After 3 weeks of follow-up, the aneurysms were occluded with Guglielmi detachable coils. They revealed that the aneurysms were completely occluded by early thrombus formation in the first 2 days after coil embolisation. Other histopathological studies have analyzed embolised aneurysms in humans. These studies revealed that blood clots were formed in the aneurysms, and fibrin coating of the coil occurred 7 days after coil embolisation was performed (4). Based on this evidence, Okamura et al. (2006) suggested that aneurysms will be fixed ~2 weeks after coil embolisation, and thus ECT can be considered at least 2 weeks after coil embolisation (5). In terms of risk management for ECT after embolisation, Okamura et al. (2006) suggested that the risk of ECT, which involves straining the wall of the aneurysm, is eliminated after the treatment for the aneurysm is completed; generally, it takes about 1 week. Therefore, theoretically, the risk of intracranial vascular complications due to ECT is low (5). In contrast, Van Herck et al. (2009) stated that blood pressure control is important when performing ECT in untreated or post-treated patients with cerebral aneurysms (2). Our anaesthesiologist monitored the patient's blood pressure before and during ECT. In conclusion, we report a case in which ECT was completed without major adverse events in a patient with DLB who was previously treated with post-coil embolisation for an aneurysm. ECT improved the patient's treatment-resistant severe depressive symptoms. It is important that ECT is performed at least 2 weeks after coil embolisation and that blood pressure is controlled. Anaesthesiologists and neurosurgeons should assess the risk of ECT and fully discuss the advantages and disadvantages of the treatment with individual patients and their family. Research data are not shared. Appendix S1. Supporting information Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article." @default.
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• W4296625101 date "2022-09-21" @default.
• W4296625101 modified "2023-10-17" @default.
• W4296625101 title "Electroconvulsive therapy for severe depressive symptoms in a patient with dementia with Lewy bodies after coil embolisation for a cerebral aneurysm" @default.
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• W4296625101 doi "https://doi.org/10.1111/psyg.12895" @default.
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