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A Case of Prolonged Catatonia Caused by Sjögren’s Syndrome

A Case of Prolonged Catatonia Caused by Sjögren’s Syndrome Hindawi Case Reports in Immunology Volume 2020, Article ID 8881503, 4 pages https://doi.org/10.1155/2020/8881503 Case Report A Case of Prolonged Catatonia Caused by Sjogren’s Syndrome 1,2 3 2,4 Takahiko Inagaki , Kotaro Kudo , Naoki Kurimoto, 2,5 2,6 Takashi Aoki, and Kenichi Kuriyama Biwako Hospital, 1-8-5, Sakamoto, Otsu, Shiga 520-0113, Japan Department of Psychiatry, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Shiga 520-2192, Japan Sanseikai Hospital, 1185, Uenohara, Uenohara, Yamanashi 409-0112, Japan Shigasato Hospital, 1-18-41, Shigasato, Otsu, Shiga 520-0006, Japan Shiga Hachiman Hospital, 744, Takakai-cho, Omihachiman, Shiga 523-0891, Japan Department of Sleep-Wake Disorders, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawa-Higashi, Kodaira, Tokyo 187-8553, Japan Correspondence should be addressed to Kenichi Kuriyama; kenichik@ncnp.go.jp Received 14 July 2020; Accepted 20 October 2020; Published 3 November 2020 Academic Editor: Rajni Rani Copyright © 2020 Takahiko Inagaki et al. (is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Sjogren’s ¨ syndrome (SS) is a chronic autoimmune disorder, often associated with some neuropsychiatric symptoms as well as systemic lupus erythematosus. Although catatonia is frequently reported in patients with systemic lupus erythematosus, it has been rarely reported in patients with SS. Herein, we present a case of SS with catatonia effectively and safely treated with modified electroconvulsive therapy (ECT). A 58-year-old woman showed prolonged catatonia and depressive mood along with patho- logically dried eye and mouth. Based on physical findings and blood tests, she was diagnosed with SS. Because of the presence of pressure sores, we were unable to perform lumbar puncture for the diagnosis of abacterial encephalitis. Alternatively, single- photon emission computed tomography of her brain revealed multifocal hypoperfused areas in the parietotemporal region. Consequently, we performed ECT for the treatment of catatonia comorbid with SS. Following 20 sessions of ECT, the catatonia was improved without obvious adverse effects. One week after the last ECT, elevated levels of interleukin-6 were identified in the cerebral fluid. After receiving steroid pulse therapy, she has not experienced catatonia for more than 5 years. SS can cause catatonia, and ECT is a safe and effective option for the treatment of catatonia with SS. It is well established that systemic lupus erythematosus 1. Introduction (SLE) is associated with a risk of developing catatonia. SLE is Catatonia is a neuropsychiatric condition characterised by often accompanied by some neuropsychiatric manifesta- physical presentations ranging from profound immobility to tions; thus, SLE comorbid with neuropsychiatric symptoms excessive motor activity. It occurs as a clinical phenotype of is termed neuropsychiatric SLE (NPSLE). Although cata- various psychiatric, neurologic, or medical conditions es- tonia is a rare neuropsychiatric symptom in SLE, it is also pecially affecting the central nervous system (CNS). It is considered a symptom of NPSLE [2]. often prolonged and accompanied by poor physical con- Sjo¨gren’s syndrome (SS) is also a chronic autoimmune ditions; therefore, appropriate and prompt medical inter- disorder, which is often associated with psychiatric conditions ventions are often required to avoid the development of (e.g., depression and anxiety disorders) [3]. Although SS shares pathological complications. Owing to its safety and effec- a similar autoimmune pathogenesis with SLE and several cases tiveness, electroconvulsive therapy (ECT) is a prime can- of NPSLE with catatonia have been reported [2, 4, 5], there is didate for treating catatonia with some comorbid medical limited knowledge regarding catatonia with SS. Herein, we conditions [1]. report a case of prolonged catatonia comorbid with SS. 2 Case Reports in Immunology disorder. Subsequently, we performed modified electro- 2. Case Presentation convulsive therapy (ECT) to treat her catatonia. A 58-year-old woman, without any past and family history She received a 20-session course of ECT within a period of psychiatric illnesses, presented with symptoms of cata- of 10 weeks. (ere were no adverse effects that interfered tonia (e.g., extreme forward inclined posture, grim ex- with the treatment, except for minor temporal delirium. Her pression, extremely low volume of voice, and limited catatonia was obviously improved along with the other speech). She appeared to have acoustic hyperesthesia be- depressive symptoms, including appetite loss and decline in cause loud conversations with individuals around her hurt locomotor activity. One week after the final ECT session, her her feelings. Hypopraxia resulted in some pressure sores on pressure sores had completely resolved, and we were able to her hips. Subsequently, she developed additional depressive collect cerebrospinal fluid through a lumbar puncture for symptoms, including depressed mood, inhibition of cytological examination. (e results showed an increased thoughts, fatigue, low self-esteem, appetite loss, and sleep cell count (10/μL), elevated IgG levels (14.3 mg/dL), and disturbances with marked psychosocial dysfunction. Her elevated interleukin-6 levels (5.14 pg/mL). (e specific family informed the medical team that her catatonic gravity and protein levels were within the normal limits. symptoms were initially observed 7 months earlier and Based on these observations, we confirmed the diagnosis of gradually worsened. She reported sharp pain in various parts neuropsychiatric SS. of her body (mainly, the back), without any causes of the Following steroid pulse therapy, she has not experienced pain that directed her to consult us. catatonia for more than 5 years without the need for psy- At the time of admission to our hospital, she had been chiatric treatments (e.g., antidepressants and ECT). receiving loxoprofen (prescribed by her family practitioner); We obtained written informed consent for publication however, she had discontinued treatment due to the absence from the patient. of analgesic effects. Blood testing did not reveal signs of infection. Also, she did not show any signs of Parkinsonism 3. Discussion other than the tonus enhancement of muscles and extreme forward inclined posture. Computed tomography and We noted two important clinical observations in this case. magnetic resonance imaging of her brain did not show any Firstly, SS can be occasionally accompanied by catatonia. albocinereous or cerebrovascular abnormalities. (ese Moreover, delayed detection and inadequate treatment of findings initially suggested that her catatonic symptoms may catatonia in the early phase could prolong and deteriorate have been caused by major depressive disorder. the general condition of the patient. In this case, we treat the However, her family had not been aware of her de- prolonged catatonia along with depressive symptoms using pressive symptoms until the catatonic symptoms became steroid pulse therapy and its maintenance therapy after a obvious. In addition, we simultaneously noticed that her course of ECT. (e patient has been free of catatonia for a eyes and mouth were extremely dry. She did not present period of >5 years. (e therapeutic course suggested that with any specific dermatological and mucosal symptoms of catatonia with depressive episodes was a consequence of SS SLE. Pleuritis and pericarditis were excluded using ultra- pathology. Although psychiatric symptoms have been sonography of the heart. Urinalysis did not demonstrate commonly reported in SS [3], to the best of our knowledge, proteinuria or cellular cast. She had leukopenia (1,500/ only one case of catatonia comorbid with SS has been mm ), but not anaemia, lymphopenia, or thrombocyto- previously reported [9]. penia. Antiphospholipid antibodies, antibodies against Secondly, ECT can be safe and effective option for the native DNA, antinuclear antibodies, or antibodies against treatment of prolonged catatonia caused by SS. SS shares a the Sm nuclear antigen were not detected. However, an- similar autoimmune pathogenesis with SLE; hence, cata- tibodies against Ro (SSA) were detected in her serum tonia with SS could be treated with ECT via similar im- sample (128 U/mL). Schirmer’s test showed positive provement mechanisms to those observed for SLE [2, 4, 5]. hypolacrimation (2 mm in 5 min). Labial gland tissue bi- Malur et al. suggested that ECT is effective for the treatment opsy showed several foci of lymphocytic sialoadenitis. of prolonged catatonia with complex medical comorbidities, According to the American College of Rheumatology but may require a higher number of treatment sessions Classification Criteria for SS [6] and Classification Criteria compared with therapy for simple catatonia [10]. (is case for SS of the American-European Consensus Group [7], we also required more ECT sessions to achieve remission of diagnosed this patient with SS. catatonia than those needed for the treatment of major Because of the presence of pressure sores, we were not depression. However, the course of ECT did not lead to any able to perform lumbar puncture for the identification of major adverse events. inflammatory pathologies in the CNS. Single-photon (is case implied that various chronic autoimmune emission computed tomography of the head showed mul- disorders potentially involve CNS pathology associated with tifocal hypoperfused areas (Figure 1). It has been reported neuropsychiatric symptoms, including catatonia. While that patchy diffuse hypoperfusion, as a manifestation of diagnosing autoimmune disorders with psychiatric symp- abacterial encephalitis, is commonly observed in patients toms, highly invasive tests, such as cerebrospinal fluid ex- with NPSLE [8]. (us, we considered she had an autoim- amination, are required. (us, when the patient is mune pathology in CNS and hypothesised that her catatonia debilitated, as in cases with catatonia, physicians must was probably caused by SS rather than major depressive sometimes prioritise empirical therapy over definitive Case Reports in Immunology 3 Figure 1: A head image of this patient obtained through single-photon emission computed tomography (SPECT). SPECT detected multifocal hypoperfused areas in the left parietotemporal region and left basal ganglia (red arrows). diagnosis to save the patient’s life. (e empirical adminis- Professor Nobuya Ishida for their insightful advice on di- tration of ECT may be relatively safe and effective for the agnosing and treating the patients. treatment of catatonia comorbid with chronic autoimmune disorders. Moreover, it may be helpful in promoting the References diagnostic process of comorbid autoimmune disorders re- sponsible for catatonia. [1] K. Brar, S. S. Kaushik, and S. Lippmann, “Catatonia update,” 4e Primary Care Companion for CNS Disorders, vol. 19, 2017. [2] A. Boeke, B. Pullen, L. Coppes, M. Medina, and J. J. Cooper, 4. Final Diagnosis “Catatonia associated with systemic lupus erythematosus (e final diagnosis was catatonia associated with Sj ogren’s ¨ (SLE): a report of two cases and a review of the literature,” Psychosomatics, vol. 59, no. 6, pp. 523–530, 2018. syndrome. [3] C.-C. Shen, A. C. Yang, B. I.-T. Kuo, and S.-J. Tsai, “Risk of psychiatric disorders following primary sjogren ¨ syndrome: a Data Availability nationwide population-based retrospective cohort study,” 4e Journal of Rheumatology, vol. 42, no. 7, pp. 1203–1208, 2015. (e clinical data used to support the findings of this study [4] A. Hussain, T. H. Mir, M. A. Dar et al., “Systemic lupus are included within the article. erythematous presenting as catatonia and its response to electroconvulie therapy,” Indian Journal of Psychological Conflicts of Interest Medicine, vol. 37, no. 4, pp. 456–459, 2015. [5] T. Leon, A. Aguirre, C. Pesce, P. Sanhueza, and P. Toro, (e authors declare that there are no conflicts of interest. “Electroconvulsive therapy for catatonia in juvenile neuro- psychiatric lupus,” Lupus, vol. 23, no. 10, pp. 1066–1068, 2014. [6] S. C. Shiboski, C. H. Shiboski, L. A. Criswell et al., “American Acknowledgments College of Rheumatology classification criteria for Sjogren’s ¨ (e authors thank their colleagues from the Department of syndrome: a data-driven, expert consensus approach in the Psychiatry, Shiga University of Medical Science, who Sjogren’s ¨ International Collaborative Clinical Alliance Co- assisted their clinical practice. (e authors also thank hort,” Arthritis Care & Research, vol. 64, no. 4, pp. 475–487, Professor Yuji Ozeki, Professor Naoto Yamada, and 2012. 4 Case Reports in Immunology [7] C. Vitali, S. Bombardieri, R. Jonsson et al., “Classification criteria for Sjogren’s syndrome: a revised version of the Eu- ropean criteria proposed by the American-European Con- sensus Group,” Annals of the Rheumatic Diseases, vol. 61, no. 6, pp. 554–558, 2002. [8] P. L. Peterson, J. S. Axford, and D. Isenberg, “Imaging in CNS lupus,” Best Practice & Research Clinical Rheumatology, vol. 19, no. 5, pp. 727–739, 2005. [9] S. N. Rosado, V. Silveira, A. I. Reis, A. Gordinho, and C. Noronha, “Catatonia and psychosis as manifestations of primary sjogren’s ¨ syndrome,” European Journal of Case Re- ports in Internal Medicine, vol. 5, no. 6, Article ID 000855, [10] C. Malur, E. Pasol, and A. Francis, “ECT for prolonged cat- atonia,” 4e Journal of ECT, vol. 17, no. 1, pp. 55–59, 2001. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Case Reports in Immunology Hindawi Publishing Corporation

A Case of Prolonged Catatonia Caused by Sjögren’s Syndrome

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Hindawi Publishing Corporation
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Copyright © 2020 Takahiko Inagaki et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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10.1155/2020/8881503
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Abstract

Hindawi Case Reports in Immunology Volume 2020, Article ID 8881503, 4 pages https://doi.org/10.1155/2020/8881503 Case Report A Case of Prolonged Catatonia Caused by Sjogren’s Syndrome 1,2 3 2,4 Takahiko Inagaki , Kotaro Kudo , Naoki Kurimoto, 2,5 2,6 Takashi Aoki, and Kenichi Kuriyama Biwako Hospital, 1-8-5, Sakamoto, Otsu, Shiga 520-0113, Japan Department of Psychiatry, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Shiga 520-2192, Japan Sanseikai Hospital, 1185, Uenohara, Uenohara, Yamanashi 409-0112, Japan Shigasato Hospital, 1-18-41, Shigasato, Otsu, Shiga 520-0006, Japan Shiga Hachiman Hospital, 744, Takakai-cho, Omihachiman, Shiga 523-0891, Japan Department of Sleep-Wake Disorders, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawa-Higashi, Kodaira, Tokyo 187-8553, Japan Correspondence should be addressed to Kenichi Kuriyama; kenichik@ncnp.go.jp Received 14 July 2020; Accepted 20 October 2020; Published 3 November 2020 Academic Editor: Rajni Rani Copyright © 2020 Takahiko Inagaki et al. (is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Sjogren’s ¨ syndrome (SS) is a chronic autoimmune disorder, often associated with some neuropsychiatric symptoms as well as systemic lupus erythematosus. Although catatonia is frequently reported in patients with systemic lupus erythematosus, it has been rarely reported in patients with SS. Herein, we present a case of SS with catatonia effectively and safely treated with modified electroconvulsive therapy (ECT). A 58-year-old woman showed prolonged catatonia and depressive mood along with patho- logically dried eye and mouth. Based on physical findings and blood tests, she was diagnosed with SS. Because of the presence of pressure sores, we were unable to perform lumbar puncture for the diagnosis of abacterial encephalitis. Alternatively, single- photon emission computed tomography of her brain revealed multifocal hypoperfused areas in the parietotemporal region. Consequently, we performed ECT for the treatment of catatonia comorbid with SS. Following 20 sessions of ECT, the catatonia was improved without obvious adverse effects. One week after the last ECT, elevated levels of interleukin-6 were identified in the cerebral fluid. After receiving steroid pulse therapy, she has not experienced catatonia for more than 5 years. SS can cause catatonia, and ECT is a safe and effective option for the treatment of catatonia with SS. It is well established that systemic lupus erythematosus 1. Introduction (SLE) is associated with a risk of developing catatonia. SLE is Catatonia is a neuropsychiatric condition characterised by often accompanied by some neuropsychiatric manifesta- physical presentations ranging from profound immobility to tions; thus, SLE comorbid with neuropsychiatric symptoms excessive motor activity. It occurs as a clinical phenotype of is termed neuropsychiatric SLE (NPSLE). Although cata- various psychiatric, neurologic, or medical conditions es- tonia is a rare neuropsychiatric symptom in SLE, it is also pecially affecting the central nervous system (CNS). It is considered a symptom of NPSLE [2]. often prolonged and accompanied by poor physical con- Sjo¨gren’s syndrome (SS) is also a chronic autoimmune ditions; therefore, appropriate and prompt medical inter- disorder, which is often associated with psychiatric conditions ventions are often required to avoid the development of (e.g., depression and anxiety disorders) [3]. Although SS shares pathological complications. Owing to its safety and effec- a similar autoimmune pathogenesis with SLE and several cases tiveness, electroconvulsive therapy (ECT) is a prime can- of NPSLE with catatonia have been reported [2, 4, 5], there is didate for treating catatonia with some comorbid medical limited knowledge regarding catatonia with SS. Herein, we conditions [1]. report a case of prolonged catatonia comorbid with SS. 2 Case Reports in Immunology disorder. Subsequently, we performed modified electro- 2. Case Presentation convulsive therapy (ECT) to treat her catatonia. A 58-year-old woman, without any past and family history She received a 20-session course of ECT within a period of psychiatric illnesses, presented with symptoms of cata- of 10 weeks. (ere were no adverse effects that interfered tonia (e.g., extreme forward inclined posture, grim ex- with the treatment, except for minor temporal delirium. Her pression, extremely low volume of voice, and limited catatonia was obviously improved along with the other speech). She appeared to have acoustic hyperesthesia be- depressive symptoms, including appetite loss and decline in cause loud conversations with individuals around her hurt locomotor activity. One week after the final ECT session, her her feelings. Hypopraxia resulted in some pressure sores on pressure sores had completely resolved, and we were able to her hips. Subsequently, she developed additional depressive collect cerebrospinal fluid through a lumbar puncture for symptoms, including depressed mood, inhibition of cytological examination. (e results showed an increased thoughts, fatigue, low self-esteem, appetite loss, and sleep cell count (10/μL), elevated IgG levels (14.3 mg/dL), and disturbances with marked psychosocial dysfunction. Her elevated interleukin-6 levels (5.14 pg/mL). (e specific family informed the medical team that her catatonic gravity and protein levels were within the normal limits. symptoms were initially observed 7 months earlier and Based on these observations, we confirmed the diagnosis of gradually worsened. She reported sharp pain in various parts neuropsychiatric SS. of her body (mainly, the back), without any causes of the Following steroid pulse therapy, she has not experienced pain that directed her to consult us. catatonia for more than 5 years without the need for psy- At the time of admission to our hospital, she had been chiatric treatments (e.g., antidepressants and ECT). receiving loxoprofen (prescribed by her family practitioner); We obtained written informed consent for publication however, she had discontinued treatment due to the absence from the patient. of analgesic effects. Blood testing did not reveal signs of infection. Also, she did not show any signs of Parkinsonism 3. Discussion other than the tonus enhancement of muscles and extreme forward inclined posture. Computed tomography and We noted two important clinical observations in this case. magnetic resonance imaging of her brain did not show any Firstly, SS can be occasionally accompanied by catatonia. albocinereous or cerebrovascular abnormalities. (ese Moreover, delayed detection and inadequate treatment of findings initially suggested that her catatonic symptoms may catatonia in the early phase could prolong and deteriorate have been caused by major depressive disorder. the general condition of the patient. In this case, we treat the However, her family had not been aware of her de- prolonged catatonia along with depressive symptoms using pressive symptoms until the catatonic symptoms became steroid pulse therapy and its maintenance therapy after a obvious. In addition, we simultaneously noticed that her course of ECT. (e patient has been free of catatonia for a eyes and mouth were extremely dry. She did not present period of >5 years. (e therapeutic course suggested that with any specific dermatological and mucosal symptoms of catatonia with depressive episodes was a consequence of SS SLE. Pleuritis and pericarditis were excluded using ultra- pathology. Although psychiatric symptoms have been sonography of the heart. Urinalysis did not demonstrate commonly reported in SS [3], to the best of our knowledge, proteinuria or cellular cast. She had leukopenia (1,500/ only one case of catatonia comorbid with SS has been mm ), but not anaemia, lymphopenia, or thrombocyto- previously reported [9]. penia. Antiphospholipid antibodies, antibodies against Secondly, ECT can be safe and effective option for the native DNA, antinuclear antibodies, or antibodies against treatment of prolonged catatonia caused by SS. SS shares a the Sm nuclear antigen were not detected. However, an- similar autoimmune pathogenesis with SLE; hence, cata- tibodies against Ro (SSA) were detected in her serum tonia with SS could be treated with ECT via similar im- sample (128 U/mL). Schirmer’s test showed positive provement mechanisms to those observed for SLE [2, 4, 5]. hypolacrimation (2 mm in 5 min). Labial gland tissue bi- Malur et al. suggested that ECT is effective for the treatment opsy showed several foci of lymphocytic sialoadenitis. of prolonged catatonia with complex medical comorbidities, According to the American College of Rheumatology but may require a higher number of treatment sessions Classification Criteria for SS [6] and Classification Criteria compared with therapy for simple catatonia [10]. (is case for SS of the American-European Consensus Group [7], we also required more ECT sessions to achieve remission of diagnosed this patient with SS. catatonia than those needed for the treatment of major Because of the presence of pressure sores, we were not depression. However, the course of ECT did not lead to any able to perform lumbar puncture for the identification of major adverse events. inflammatory pathologies in the CNS. Single-photon (is case implied that various chronic autoimmune emission computed tomography of the head showed mul- disorders potentially involve CNS pathology associated with tifocal hypoperfused areas (Figure 1). It has been reported neuropsychiatric symptoms, including catatonia. While that patchy diffuse hypoperfusion, as a manifestation of diagnosing autoimmune disorders with psychiatric symp- abacterial encephalitis, is commonly observed in patients toms, highly invasive tests, such as cerebrospinal fluid ex- with NPSLE [8]. (us, we considered she had an autoim- amination, are required. (us, when the patient is mune pathology in CNS and hypothesised that her catatonia debilitated, as in cases with catatonia, physicians must was probably caused by SS rather than major depressive sometimes prioritise empirical therapy over definitive Case Reports in Immunology 3 Figure 1: A head image of this patient obtained through single-photon emission computed tomography (SPECT). SPECT detected multifocal hypoperfused areas in the left parietotemporal region and left basal ganglia (red arrows). diagnosis to save the patient’s life. (e empirical adminis- Professor Nobuya Ishida for their insightful advice on di- tration of ECT may be relatively safe and effective for the agnosing and treating the patients. treatment of catatonia comorbid with chronic autoimmune disorders. Moreover, it may be helpful in promoting the References diagnostic process of comorbid autoimmune disorders re- sponsible for catatonia. [1] K. Brar, S. S. Kaushik, and S. Lippmann, “Catatonia update,” 4e Primary Care Companion for CNS Disorders, vol. 19, 2017. [2] A. Boeke, B. Pullen, L. Coppes, M. Medina, and J. J. Cooper, 4. Final Diagnosis “Catatonia associated with systemic lupus erythematosus (e final diagnosis was catatonia associated with Sj ogren’s ¨ (SLE): a report of two cases and a review of the literature,” Psychosomatics, vol. 59, no. 6, pp. 523–530, 2018. syndrome. [3] C.-C. Shen, A. C. Yang, B. I.-T. Kuo, and S.-J. Tsai, “Risk of psychiatric disorders following primary sjogren ¨ syndrome: a Data Availability nationwide population-based retrospective cohort study,” 4e Journal of Rheumatology, vol. 42, no. 7, pp. 1203–1208, 2015. (e clinical data used to support the findings of this study [4] A. Hussain, T. H. Mir, M. A. Dar et al., “Systemic lupus are included within the article. erythematous presenting as catatonia and its response to electroconvulie therapy,” Indian Journal of Psychological Conflicts of Interest Medicine, vol. 37, no. 4, pp. 456–459, 2015. [5] T. Leon, A. Aguirre, C. Pesce, P. Sanhueza, and P. Toro, (e authors declare that there are no conflicts of interest. “Electroconvulsive therapy for catatonia in juvenile neuro- psychiatric lupus,” Lupus, vol. 23, no. 10, pp. 1066–1068, 2014. [6] S. C. Shiboski, C. H. Shiboski, L. A. Criswell et al., “American Acknowledgments College of Rheumatology classification criteria for Sjogren’s ¨ (e authors thank their colleagues from the Department of syndrome: a data-driven, expert consensus approach in the Psychiatry, Shiga University of Medical Science, who Sjogren’s ¨ International Collaborative Clinical Alliance Co- assisted their clinical practice. (e authors also thank hort,” Arthritis Care & Research, vol. 64, no. 4, pp. 475–487, Professor Yuji Ozeki, Professor Naoto Yamada, and 2012. 4 Case Reports in Immunology [7] C. Vitali, S. Bombardieri, R. Jonsson et al., “Classification criteria for Sjogren’s syndrome: a revised version of the Eu- ropean criteria proposed by the American-European Con- sensus Group,” Annals of the Rheumatic Diseases, vol. 61, no. 6, pp. 554–558, 2002. [8] P. L. Peterson, J. S. Axford, and D. Isenberg, “Imaging in CNS lupus,” Best Practice & Research Clinical Rheumatology, vol. 19, no. 5, pp. 727–739, 2005. [9] S. N. Rosado, V. Silveira, A. I. Reis, A. Gordinho, and C. Noronha, “Catatonia and psychosis as manifestations of primary sjogren’s ¨ syndrome,” European Journal of Case Re- ports in Internal Medicine, vol. 5, no. 6, Article ID 000855, [10] C. Malur, E. Pasol, and A. Francis, “ECT for prolonged cat- atonia,” 4e Journal of ECT, vol. 17, no. 1, pp. 55–59, 2001.

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Case Reports in ImmunologyHindawi Publishing Corporation

Published: Nov 3, 2020

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