Pub Date : 2024-12-07eCollection Date: 2024-01-01DOI: 10.1155/crps/8870476
Richard C J Bradlow, Sophie Wright, Anamaria Szrajbman Vaz Da Silva, Ferghal Armstrong
Introduction: There has been a recent significant increase in medical cannabis prescribing in Australia despite weak evidence for its effectiveness in treating the most common indications. Concern has been raised about the potential harms of inappropriate prescription of cannabis; however, there have been no prior published cases of psychosis secondary to medicinal cannabis in Australia. Case Presentation: We present a case of a 21-year-old Indigenous male with psychosis following switching from illicitly obtained cannabis to prescription cannabis, which resulted in Othello delusions towards his partner, violence towards her and ultimately an attempt to end his life. Discussion: Cannabis use is linked to the development of a psychotic illness whether it is prescribed or obtained illicitly. People who are prescribed cannabis are also at an elevated risk of developing cannabis use disorder (CUD). Cannabis prescribers need to screen for risk factors of drug-induced psychosis such as a family member with a psychotic illness, review patients regularly and provide harm minimisation advice to prevent damage from their prescription. Conclusion: There are clear dangers to overprescribing medicinal cannabis and the care that needs to be taken by prescribers to avoid them. There is a need for a change in the regulation of cannabis prescribing in Australia. Further research is warranted on the effects of the increase in prevalence of cannabis prescribing.
{"title":"High Prescribing: A Case Study of High-Potency Medicinal Cannabis Inducing Psychosis.","authors":"Richard C J Bradlow, Sophie Wright, Anamaria Szrajbman Vaz Da Silva, Ferghal Armstrong","doi":"10.1155/crps/8870476","DOIUrl":"10.1155/crps/8870476","url":null,"abstract":"<p><p><b>Introduction:</b> There has been a recent significant increase in medical cannabis prescribing in Australia despite weak evidence for its effectiveness in treating the most common indications. Concern has been raised about the potential harms of inappropriate prescription of cannabis; however, there have been no prior published cases of psychosis secondary to medicinal cannabis in Australia. <b>Case Presentation:</b> We present a case of a 21-year-old Indigenous male with psychosis following switching from illicitly obtained cannabis to prescription cannabis, which resulted in Othello delusions towards his partner, violence towards her and ultimately an attempt to end his life. <b>Discussion:</b> Cannabis use is linked to the development of a psychotic illness whether it is prescribed or obtained illicitly. People who are prescribed cannabis are also at an elevated risk of developing cannabis use disorder (CUD). Cannabis prescribers need to screen for risk factors of drug-induced psychosis such as a family member with a psychotic illness, review patients regularly and provide harm minimisation advice to prevent damage from their prescription. <b>Conclusion:</b> There are clear dangers to overprescribing medicinal cannabis and the care that needs to be taken by prescribers to avoid them. There is a need for a change in the regulation of cannabis prescribing in Australia. Further research is warranted on the effects of the increase in prevalence of cannabis prescribing.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"8870476"},"PeriodicalIF":0.0,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11646144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-26eCollection Date: 2024-01-01DOI: 10.1155/crps/6452923
Danyaal Khan, Christie Richardson, Martin Forsberg
Nightmares and flashbacks are common debilitating symptoms of posttraumatic stress disorder (PTSD) that can disrupt daily functioning. Prazosin, an alpha-1 adrenergic antagonist, has been commonly used off-label for the treatment of these intrusion symptoms, although its short half-life makes it so that often multiple doses are needed. Doxazosin, another alpha-1 antagonist, is starting to be investigated in the treatment of PTSD-related nightmares due to its lesser side effect profile and longer half-life. In our case series, we present three cases of patients with PTSD-related nightmares who were successfully treated with doxazosin following a relapse of symptoms after discontinuation of prazosin for various reasons. The success of doxazosin immediate release for PTSD-related nightmares warrants further studies into its efficacy and use as an alternative treatment to prazosin.
{"title":"Doxazosin Immediate Release as a Novel Treatment for Nightmares in Posttraumatic Stress Disorder.","authors":"Danyaal Khan, Christie Richardson, Martin Forsberg","doi":"10.1155/crps/6452923","DOIUrl":"10.1155/crps/6452923","url":null,"abstract":"<p><p>Nightmares and flashbacks are common debilitating symptoms of posttraumatic stress disorder (PTSD) that can disrupt daily functioning. Prazosin, an alpha-1 adrenergic antagonist, has been commonly used off-label for the treatment of these intrusion symptoms, although its short half-life makes it so that often multiple doses are needed. Doxazosin, another alpha-1 antagonist, is starting to be investigated in the treatment of PTSD-related nightmares due to its lesser side effect profile and longer half-life. In our case series, we present three cases of patients with PTSD-related nightmares who were successfully treated with doxazosin following a relapse of symptoms after discontinuation of prazosin for various reasons. The success of doxazosin immediate release for PTSD-related nightmares warrants further studies into its efficacy and use as an alternative treatment to prazosin.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"6452923"},"PeriodicalIF":0.0,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11614496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-23eCollection Date: 2024-01-01DOI: 10.1155/2024/6638911
Faisal R Elali, Arthur C Grant
Bupropion is an atypical antidepressant indicated for the treatment of major depressive disorder (MDD), seasonal affective disorder (SAD), and smoking cessation. It is also used off-label for attention deficit hyperactivity disorder (ADHD). Its mechanism of action includes the selective norepinephrine and dopamine reuptake inhibitor (NDRI). The drug is available in immediate-release (IR), sustained-release (SR), and extended-release (XL) formulations. Common side effects are typically mild and include anxiety, insomnia, headache, dizziness, constipation, and nausea. Rarely, cutaneous hypersensitivity reactions may occur. We describe a 23-year-old man who developed severe and diffuse urticaria and angioedema 4 weeks after initiation of bupropion XL for MDD and ADHD. The bupropion was stopped, and he was treated with levocetirizine, diphenhydramine (oral and topical), and methylprednisolone with complete resolution of his symptoms within 2 weeks. Due to a good initial therapeutic response to the medication, a trial of bupropion SR was initiated. The patient again had a favorable therapeutic response without any dermatologic side effects.
{"title":"Tolerance of Bupropion SR After Delayed-Onset Urticaria and Angioedema Associated With Bupropion XL.","authors":"Faisal R Elali, Arthur C Grant","doi":"10.1155/2024/6638911","DOIUrl":"10.1155/2024/6638911","url":null,"abstract":"<p><p>Bupropion is an atypical antidepressant indicated for the treatment of major depressive disorder (MDD), seasonal affective disorder (SAD), and smoking cessation. It is also used off-label for attention deficit hyperactivity disorder (ADHD). Its mechanism of action includes the selective norepinephrine and dopamine reuptake inhibitor (NDRI). The drug is available in immediate-release (IR), sustained-release (SR), and extended-release (XL) formulations. Common side effects are typically mild and include anxiety, insomnia, headache, dizziness, constipation, and nausea. Rarely, cutaneous hypersensitivity reactions may occur. We describe a 23-year-old man who developed severe and diffuse urticaria and angioedema 4 weeks after initiation of bupropion XL for MDD and ADHD. The bupropion was stopped, and he was treated with levocetirizine, diphenhydramine (oral and topical), and methylprednisolone with complete resolution of his symptoms within 2 weeks. Due to a good initial therapeutic response to the medication, a trial of bupropion SR was initiated. The patient again had a favorable therapeutic response without any dermatologic side effects.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"6638911"},"PeriodicalIF":0.0,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11524701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-26eCollection Date: 2024-01-01DOI: 10.1155/2024/6728600
Jonatan Escobar-Herrera, Gibran Raymundo León-Gallegos, Omar E Valencia-Ledezma, Rafael García-Rascon, Nicolás Santiago-González
Delusional parasitosis is a psychotic disorder where the patient has the delusion of being infested with some insect or parasite. In contrast, shared paranoid disorder or folie à deux is described when the same delusions affect two or more closely related people. It is common for these two situations to cause comorbidity in the family unit. This case report concerns a couple married for 37 years. The husband described that 2 years ago, he began with a tingling sensation throughout his body, related to the presence of parasites coming out from all his body orifices, with no evidence of self-harm. Likewise, the wife reported symptoms of formication and the feeling that there were invisible animals, as mentioned by her husband, and that she felt the parasites running throughout her body. The husband was diagnosed with endoparasitic delusional parasitosis, which caused folie à deux in his wife due to ectoparasitic parasitosis. The patient's treatment included sertraline and risperidone in oral dosage lasting 3 months reducing delirium, later biperidene was prescribed due to main treatment's side effects such as akathisia and sialorrhea, however the patient could not take the medication due to economic reasons. The wife was asked to sleep in a separate room, and she reported that the sensory hallucinations disappeared as soon as she slept in a different room. We conclude that the pharmacological approach, the intervention in the family life, and the gradual reintegration of marital habits once the patient improves are crucial in the therapy of delusional disorder.
{"title":"Delusional Parasitosis in Comorbidity With Shared Paranoid Disorder in a Marriage.","authors":"Jonatan Escobar-Herrera, Gibran Raymundo León-Gallegos, Omar E Valencia-Ledezma, Rafael García-Rascon, Nicolás Santiago-González","doi":"10.1155/2024/6728600","DOIUrl":"10.1155/2024/6728600","url":null,"abstract":"<p><p>Delusional parasitosis is a psychotic disorder where the patient has the delusion of being infested with some insect or parasite. In contrast, shared paranoid disorder or folie à deux is described when the same delusions affect two or more closely related people. It is common for these two situations to cause comorbidity in the family unit. This case report concerns a couple married for 37 years. The husband described that 2 years ago, he began with a tingling sensation throughout his body, related to the presence of parasites coming out from all his body orifices, with no evidence of self-harm. Likewise, the wife reported symptoms of formication and the feeling that there were invisible animals, as mentioned by her husband, and that she felt the parasites running throughout her body. The husband was diagnosed with endoparasitic delusional parasitosis, which caused folie à deux in his wife due to ectoparasitic parasitosis. The patient's treatment included sertraline and risperidone in oral dosage lasting 3 months reducing delirium, later biperidene was prescribed due to main treatment's side effects such as akathisia and sialorrhea, however the patient could not take the medication due to economic reasons. The wife was asked to sleep in a separate room, and she reported that the sensory hallucinations disappeared as soon as she slept in a different room. We conclude that the pharmacological approach, the intervention in the family life, and the gradual reintegration of marital habits once the patient improves are crucial in the therapy of delusional disorder.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"6728600"},"PeriodicalIF":0.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11449551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-25eCollection Date: 2024-01-01DOI: 10.1155/2024/5535830
Annelien Marcelis, Evelyne Van Reet
Kinesin family member 11 (KIF11)-associated disorder, a rare condition caused by autosomal dominant mutations in the KIF11 gene, presents with microcephaly, chorioretinal dysplasia, lymphoedema, and varying degrees of intellectual disability. While intellectual disability is often described in the literature on KIF11 mutations, autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are only mentioned by a few authors but not thoroughly investigated. We present a case report of an 8-year-old boy with KIF11-associated disorder alongside ADHD and ASD but without intellectual disability. Genetic testing confirmed a KIF11 mutation. Cognitive, language, and motor assessments revealed delays in fine motor skills and attention deficits. The diagnosis of ADHD was confirmed by a child neurologist through multidisciplinary investigations, while the ASD diagnosis was established by a child psychiatrist. Despite the challenges of delayed psychiatric assessment, interventions including physiotherapy and medication management were initiated with positive results. We designed a parent support group survey that showed a higher prevalence of neurodevelopmental disorders in children with KIF11 mutations compared to the general population. Therefore, low-threshold referrals to a child psychiatrist have to be made when the potential presence of developmental problems is suspected. Collaboration between ophthalmologists, paediatricians, and child psychiatrists is crucial for early detection and intervention. Addressing developmental disorders promptly improves long-term outcomes and enhances quality of life. Moreover, gaining a deeper understanding of the higher prevalence of ASD and ADHD in individuals with KIF11 mutations could offer valuable insights into the genetic mechanisms underlying neurodevelopmental disorders.
{"title":"A Boy With KIF11-Associated Disorder Along With ADHD and ASD: Collaboration Between Paediatrics and Child Psychiatry.","authors":"Annelien Marcelis, Evelyne Van Reet","doi":"10.1155/2024/5535830","DOIUrl":"10.1155/2024/5535830","url":null,"abstract":"<p><p>Kinesin family member 11 (KIF11)-associated disorder, a rare condition caused by autosomal dominant mutations in the KIF11 gene, presents with microcephaly, chorioretinal dysplasia, lymphoedema, and varying degrees of intellectual disability. While intellectual disability is often described in the literature on KIF11 mutations, autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are only mentioned by a few authors but not thoroughly investigated. We present a case report of an 8-year-old boy with KIF11-associated disorder alongside ADHD and ASD but without intellectual disability. Genetic testing confirmed a KIF11 mutation. Cognitive, language, and motor assessments revealed delays in fine motor skills and attention deficits. The diagnosis of ADHD was confirmed by a child neurologist through multidisciplinary investigations, while the ASD diagnosis was established by a child psychiatrist. Despite the challenges of delayed psychiatric assessment, interventions including physiotherapy and medication management were initiated with positive results. We designed a parent support group survey that showed a higher prevalence of neurodevelopmental disorders in children with KIF11 mutations compared to the general population. Therefore, low-threshold referrals to a child psychiatrist have to be made when the potential presence of developmental problems is suspected. Collaboration between ophthalmologists, paediatricians, and child psychiatrists is crucial for early detection and intervention. Addressing developmental disorders promptly improves long-term outcomes and enhances quality of life. Moreover, gaining a deeper understanding of the higher prevalence of ASD and ADHD in individuals with KIF11 mutations could offer valuable insights into the genetic mechanisms underlying neurodevelopmental disorders.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"5535830"},"PeriodicalIF":0.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-20eCollection Date: 2024-01-01DOI: 10.1155/2024/8845349
Mohamed Salih, Reem Mohamed Osman, Wala Alim, Leena Khalid, Wafa Sosal, Danya Ibrahim, Yassir Mahgoub
Agitated depression, also known as melancholia agitata, is a variant of depression characterized by severe symptoms of psychomotor agitation, inner unrest, anxiety, restlessness, prominent vegetative symptoms, and a high risk of suicide. This form of depression is reported to worsen with antidepressants and potentially improve with the use of ECT, lithium, antiepileptics, antipsychotics, and benzodiazepines. We describe a case of a 73-year-old female with a prior history of depression and generalized anxiety disorder who was maintained on flurazepam for 44 years and was admitted for severe depression with psychomotor agitation, prominent vegetative symptoms, thought perseveration, indecisiveness, and psychotic features that emerged following the discontinuation of flurazepam. Symptoms did not resolve with the use of alternative benzodiazepines such as nitrazepam and temazepam and further worsened with the use of several antidepressants. She finally had a complete resolution of these symptoms with a combination of alprazolam, zopiclone, and olanzapine. This case provides insight into this unique variant of depression and the role of GABA agonists in its pathology and management.
{"title":"Agitated Depression Associated With Flurazepam Discontinuation.","authors":"Mohamed Salih, Reem Mohamed Osman, Wala Alim, Leena Khalid, Wafa Sosal, Danya Ibrahim, Yassir Mahgoub","doi":"10.1155/2024/8845349","DOIUrl":"https://doi.org/10.1155/2024/8845349","url":null,"abstract":"<p><p>Agitated depression, also known as melancholia agitata, is a variant of depression characterized by severe symptoms of psychomotor agitation, inner unrest, anxiety, restlessness, prominent vegetative symptoms, and a high risk of suicide. This form of depression is reported to worsen with antidepressants and potentially improve with the use of ECT, lithium, antiepileptics, antipsychotics, and benzodiazepines. We describe a case of a 73-year-old female with a prior history of depression and generalized anxiety disorder who was maintained on flurazepam for 44 years and was admitted for severe depression with psychomotor agitation, prominent vegetative symptoms, thought perseveration, indecisiveness, and psychotic features that emerged following the discontinuation of flurazepam. Symptoms did not resolve with the use of alternative benzodiazepines such as nitrazepam and temazepam and further worsened with the use of several antidepressants. She finally had a complete resolution of these symptoms with a combination of alprazolam, zopiclone, and olanzapine. This case provides insight into this unique variant of depression and the role of GABA agonists in its pathology and management.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"8845349"},"PeriodicalIF":0.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11436266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-26eCollection Date: 2024-01-01DOI: 10.1155/2024/8827460
R Rijal, P Pokhrel
Phagophobia is a rare and debilitating mental health condition characterized by an intense fear of choking solid food or liquids. Usually there is no underlying anatomical or physiological abnormalities. Choking phobia can lead to the avoidance of solid foods and liquids. This can give rise to other psychiatric disorders like major depressive disorder and anxiety disorder. Only few case reports of choking phobia are available in the literature. Here we present the case of a middle-aged man, with a 10-year history of fear of choking, starting after an aspiration episode and later maintained by a similar episode. The patient felt that food would be stuck in the windpipe, and he could not breathe while swallowing solid food and liquids. This eventually led to reduced eating and drinking causing significant weight loss. He also isolated himself and became depressed. After several searches for help in somatic healthcare, including surgery for deviated nasal septum, the patient was finally investigated in a psychiatric clinic and treated with pharmacological measures and behavioral therapy with considerable improvement within a few months. Choking phobia can mimic different physical conditions and is often misdiagnosed. Early recognition and timely referral to mental health professionals are vital for effective management.
{"title":"Conquering Phagophobia: A Journey to Overcoming the Fear of Choking.","authors":"R Rijal, P Pokhrel","doi":"10.1155/2024/8827460","DOIUrl":"10.1155/2024/8827460","url":null,"abstract":"<p><p>Phagophobia is a rare and debilitating mental health condition characterized by an intense fear of choking solid food or liquids. Usually there is no underlying anatomical or physiological abnormalities. Choking phobia can lead to the avoidance of solid foods and liquids. This can give rise to other psychiatric disorders like major depressive disorder and anxiety disorder. Only few case reports of choking phobia are available in the literature. Here we present the case of a middle-aged man, with a 10-year history of fear of choking, starting after an aspiration episode and later maintained by a similar episode. The patient felt that food would be stuck in the windpipe, and he could not breathe while swallowing solid food and liquids. This eventually led to reduced eating and drinking causing significant weight loss. He also isolated himself and became depressed. After several searches for help in somatic healthcare, including surgery for deviated nasal septum, the patient was finally investigated in a psychiatric clinic and treated with pharmacological measures and behavioral therapy with considerable improvement within a few months. Choking phobia can mimic different physical conditions and is often misdiagnosed. Early recognition and timely referral to mental health professionals are vital for effective management.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"8827460"},"PeriodicalIF":0.0,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-23eCollection Date: 2024-01-01DOI: 10.1155/2024/6938553
Shahzaib Khan, Breanna Wennberg, Malgorzata Witkowska, Jacob Rattin, Raunak Khisty
Serotonin syndrome is a toxidrome consisting of autonomic instability, altered mentation, hyperreflexia, clonus, and seizures. It is suspected to be due to either elevated serotonin concentrations or overstimulation of 5-hydroxytryptamine (5-HT) receptors. There are at least seven families of serotonin or 5-HT receptors along with multiple subtypes. The 5-HT1A and 5-HT2A serotonin receptor subtypes are heavily suspected to cause the broad spectrum of symptoms seen in serotonin syndrome. We present the case of a young woman treated with multiple psychotropic medications who developed serotonin syndrome (SS) after receiving electroconvulsive therapy (ECT). She had multiple psychiatric hospitalizations, and ECT was determined to be the appropriate course of treatment due to her treatment-resistant symptoms and catatonia. The case was unique as she tolerated multiple ECT treatments over a few weeks before the acute onset of serotonin syndrome following her eighth treatment, and she did not have any medication changes after the second ECT treatment. The patient's acute presentation of rigidity, elevated temperature, hyperreflexia, diaphoresis, confusion, and psychomotor agitation led to a diagnosis of serotonin syndrome. ECT is a neuromodulatory procedure approved for treatment-resistant depression and schizophrenia that involves electrically stimulating the brain with electrodes on the scalp to induce a seizure. The mechanism by which ECT confers therapeutic benefit for patients with neuropsychiatric conditions is not entirely understood. We discuss some of the literature on SS and ECT to better understand the potential for a causal relationship.
血清素综合征是一种由自主神经不稳定、精神改变、反射亢进、阵挛和癫痫发作组成的中毒综合征。它被怀疑是由于血清素浓度升高或过度刺激 5-羟色胺(5-HT)受体所致。血清素或 5-HT 受体至少有七个家族和多种亚型。5-HT1A和5-HT2A血清素受体亚型很有可能导致血清素综合征的广泛症状。我们介绍了一例年轻女性的病例,她曾接受多种精神药物治疗,在接受电休克疗法(ECT)后出现了血清素综合征(SS)。她曾多次因精神疾病住院治疗,由于她的治疗耐药症状和紧张症,电休克疗法被确定为适当的治疗方案。该病例的特殊之处在于,在第八次治疗后出现血清素综合征急性发作之前,她在数周内耐受了多次电痉挛治疗,并且在第二次电痉挛治疗后没有更换任何药物。患者急性期表现为身体僵硬、体温升高、反射亢进、全身舒张、意识模糊和精神运动性躁动,因此被诊断为血清素综合征。电痉挛疗法是一种神经调节程序,已被批准用于治疗耐药抑郁症和精神分裂症,即通过头皮上的电极对大脑进行电刺激,诱发癫痫发作。ECT 为神经精神疾病患者带来治疗益处的机制尚不完全清楚。我们讨论了有关 SS 和 ECT 的一些文献,以更好地了解两者之间可能存在的因果关系。
{"title":"An Unexpected Presentation of Serotonin Syndrome in a Patient Receiving ECT.","authors":"Shahzaib Khan, Breanna Wennberg, Malgorzata Witkowska, Jacob Rattin, Raunak Khisty","doi":"10.1155/2024/6938553","DOIUrl":"10.1155/2024/6938553","url":null,"abstract":"<p><p>Serotonin syndrome is a toxidrome consisting of autonomic instability, altered mentation, hyperreflexia, clonus, and seizures. It is suspected to be due to either elevated serotonin concentrations or overstimulation of 5-hydroxytryptamine (5-HT) receptors. There are at least seven families of serotonin or 5-HT receptors along with multiple subtypes. The 5-HT<sub>1A</sub> and 5-HT<sub>2A</sub> serotonin receptor subtypes are heavily suspected to cause the broad spectrum of symptoms seen in serotonin syndrome. We present the case of a young woman treated with multiple psychotropic medications who developed serotonin syndrome (SS) after receiving electroconvulsive therapy (ECT). She had multiple psychiatric hospitalizations, and ECT was determined to be the appropriate course of treatment due to her treatment-resistant symptoms and catatonia. The case was unique as she tolerated multiple ECT treatments over a few weeks before the acute onset of serotonin syndrome following her eighth treatment, and she did not have any medication changes after the second ECT treatment. The patient's acute presentation of rigidity, elevated temperature, hyperreflexia, diaphoresis, confusion, and psychomotor agitation led to a diagnosis of serotonin syndrome. ECT is a neuromodulatory procedure approved for treatment-resistant depression and schizophrenia that involves electrically stimulating the brain with electrodes on the scalp to induce a seizure. The mechanism by which ECT confers therapeutic benefit for patients with neuropsychiatric conditions is not entirely understood. We discuss some of the literature on SS and ECT to better understand the potential for a causal relationship.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"6938553"},"PeriodicalIF":0.0,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-19eCollection Date: 2024-01-01DOI: 10.1155/2024/2863662
Megan Selig, Gloria Lee, Brian Lebowitz, Dinko Franceschi, Nicole Absar
Background: The differential diagnosis of a patient with cognitive, behavioral, and motor symptoms is broad. There is much overlap between neurocognitive disorders due to frontotemporal dementia and other subcortical dementia. A less known diagnosis, cerebellar cognitive affective syndrome (CCAS), should also be considered. Case History. A 29-year-old female presented with ataxia and left-sided weakness. CSF showed oligoclonal bands, and MRI showed multiple white matter lesions with some atrophy. She was diagnosed with multiple sclerosis (MS). At age 35, she developed frontal lobe symptoms and executive dysfunction; she was diagnosed with MS with bipolar disorder. Neuropsychological evaluation at that time showed significant deficits in multiple cognitive domains. Subsequent MRI showed progressive frontotemporal atrophy, and FDG-PET uncovered hypometabolism in the frontotemporal lobes and cerebellum. At age 38, her behavior worsened with aggression, and she was started on olanzapine. She responded well with decreased agitation and improved motivation and attention. Compared with previous scans, most recent MRI and FDG-PET showed interval increase in cerebellar atrophy with increase in hypometabolism in the cerebellum, respectively.
Conclusion: Based on cerebellar, affective, and subcortical cognitive examination findings, our diagnosis is probable CCAS. The cerebellum should be considered as a possible etiology of frontal subcortical cognitive impairment.
{"title":"A Case of Personality and Behavioral Changes with Frontotemporal and Cerebellar Atrophy on MRI with Corresponding Hypometabolism on FDG-PET.","authors":"Megan Selig, Gloria Lee, Brian Lebowitz, Dinko Franceschi, Nicole Absar","doi":"10.1155/2024/2863662","DOIUrl":"10.1155/2024/2863662","url":null,"abstract":"<p><strong>Background: </strong>The differential diagnosis of a patient with cognitive, behavioral, and motor symptoms is broad. There is much overlap between neurocognitive disorders due to frontotemporal dementia and other subcortical dementia. A less known diagnosis, cerebellar cognitive affective syndrome (CCAS), should also be considered. <i>Case History</i>. A 29-year-old female presented with ataxia and left-sided weakness. CSF showed oligoclonal bands, and MRI showed multiple white matter lesions with some atrophy. She was diagnosed with multiple sclerosis (MS). At age 35, she developed frontal lobe symptoms and executive dysfunction; she was diagnosed with MS with bipolar disorder. Neuropsychological evaluation at that time showed significant deficits in multiple cognitive domains. Subsequent MRI showed progressive frontotemporal atrophy, and FDG-PET uncovered hypometabolism in the frontotemporal lobes and cerebellum. At age 38, her behavior worsened with aggression, and she was started on olanzapine. She responded well with decreased agitation and improved motivation and attention. Compared with previous scans, most recent MRI and FDG-PET showed interval increase in cerebellar atrophy with increase in hypometabolism in the cerebellum, respectively.</p><p><strong>Conclusion: </strong>Based on cerebellar, affective, and subcortical cognitive examination findings, our diagnosis is probable CCAS. The cerebellum should be considered as a possible etiology of frontal subcortical cognitive impairment.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"2863662"},"PeriodicalIF":0.0,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11347030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-07eCollection Date: 2024-01-01DOI: 10.1155/2024/7416277
Omkar Dhungel, Indra Prasad Amatya, Pawan Sharma
Background: Hyperpigmentation is a common side effect of different drugs with many of these having a well-explained mechanism and some even having a characteristic distribution. However, it is a rare side effect of sertraline, a selective serotonin reuptake inhibitor (SSRI), with only a few reported cases. In addition, there are no specific characteristics of the lesions or the risk factors. Case Summary. This is a case report of a 24-year-old male with panic disorder, who developed hyperpigmentation over the face after 5 days of increasing the dosage of sertraline to 100 mg/day. There were no other significant findings from the physical examination or investigations. The patient was treated as a case of sertraline-induced hyperpigmentation, and the dose was reduced to 75 mg/day and maintained at 50 mg/day after 1 week along with tablet propranolol 20 mg/day. He was also prescribed tablet tranexamic acid 500 mg/day and sunscreen with sun protection factor 50. The hyperpigmentation disappeared within 2 months, and the medication was gradually tapered after 7 months of treatment.
Conclusion: Hyperpigmentation is a rare but distressing side effect of sertraline. It is a potentially curable side effect if recognized early. Early recognition and intervention can decrease unnecessary investigations and treatment. There are limited studies highlighting this unusual adverse effect of this commonly used SSRI. Hence, further studies are needed to better understand various aspects of this condition including the characteristics, patients at risk, and possible management. The development of diagnostic and treatment guidelines would decrease the dilemma of identification and management.
{"title":"An Unusual Presentation with Facial Hyperpigmentation on Escalation of the Dose of Sertraline.","authors":"Omkar Dhungel, Indra Prasad Amatya, Pawan Sharma","doi":"10.1155/2024/7416277","DOIUrl":"10.1155/2024/7416277","url":null,"abstract":"<p><strong>Background: </strong>Hyperpigmentation is a common side effect of different drugs with many of these having a well-explained mechanism and some even having a characteristic distribution. However, it is a rare side effect of sertraline, a selective serotonin reuptake inhibitor (SSRI), with only a few reported cases. In addition, there are no specific characteristics of the lesions or the risk factors. <i>Case Summary</i>. This is a case report of a 24-year-old male with panic disorder, who developed hyperpigmentation over the face after 5 days of increasing the dosage of sertraline to 100 mg/day. There were no other significant findings from the physical examination or investigations. The patient was treated as a case of sertraline-induced hyperpigmentation, and the dose was reduced to 75 mg/day and maintained at 50 mg/day after 1 week along with tablet propranolol 20 mg/day. He was also prescribed tablet tranexamic acid 500 mg/day and sunscreen with sun protection factor 50. The hyperpigmentation disappeared within 2 months, and the medication was gradually tapered after 7 months of treatment.</p><p><strong>Conclusion: </strong>Hyperpigmentation is a rare but distressing side effect of sertraline. It is a potentially curable side effect if recognized early. Early recognition and intervention can decrease unnecessary investigations and treatment. There are limited studies highlighting this unusual adverse effect of this commonly used SSRI. Hence, further studies are needed to better understand various aspects of this condition including the characteristics, patients at risk, and possible management. The development of diagnostic and treatment guidelines would decrease the dilemma of identification and management.</p>","PeriodicalId":9631,"journal":{"name":"Case Reports in Psychiatry","volume":"2024 ","pages":"7416277"},"PeriodicalIF":0.0,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11325013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}