Frontiers in Psychiatry is proud to present our Case Reports series. Our case reports aim to highlight unique cases of patients that present with an unexpected/unusual diagnosis, treatment outcome, or clinical course. Case reports provide insight into the differential diagnosis, decision making, and clinical management of unusual cases and are a valuable educational tool. This Research Topic will only accept Case Reports or Community Case Studies but also relevant Opinions and Perspectives may be considered, all manuscripts must be original with the aim to significantly advance the field to be considered. We welcome contributions that cover all aspects of Addictive Disorders.

West Virginia University

University of Macau

Baylor College of Medicine

Chinese Academy of Education Big Data, Qufu Normal University

Virginia Commonwealth University

University of Arkansas at Little Rock

Frontiers in Psychiatry

Addictive Disorders

Case Reports in Addictive Disorders

BackgroundAreca Nut (AN) is the fourth most commonly abused drug after nicotine, ethanol, and caffeine, due to its psychoactive properties provided by bioactive substances. Although previous studies have demonstrated AN’s anxiolytic-like activity and potential benefits in ameliorating symptoms of depression and schizophrenia, there remains limited awareness regarding its association with brief psychotic disorder.</sec>Case presentationThis case report presents the clinical profile of a 30-year-old male patient with a history of betel nut chewing for the past 2 years, who exhibited sudden onset delusions, hallucinations, and disorganized speech and behavior upon increasing the dosage of betel nut consumption. The patient displayed a positive response to antipsychotic treatment, and symptoms resolved upon discontinuation of betel nut consumption. However, one month after discharge, the patient experienced a recurrence of auditory hallucinations upon resuming betel nut chewing. Through counseling and support, the importance of abstaining from betel nut use and maintaining medication compliance was emphasized, resulting in no recurrence of psychotic symptoms during the six-month follow-up.</sec>ConclusionsThis case report highlights the related role of betel nut with brief psychotic disorder, especially when the chewing dosage is abruptly increased. It underscores the importance of considering betel nut as a potential precipitant related to acute psychiatric disorders in clinical settings.</sec>

Background: Areca Nut (AN) is the fourth most commonly abused drug after nicotine, ethanol, and caffeine, due to its psychoactive properties provided by bioactive substances. Although previous studies have demonstrated AN’s anxiolytic-like activity and potential benefits in ameliorating symptoms of depression and schizophrenia, there remains limited awareness regarding its association with brief psychotic disorder.Case presentation: This case report presents the clinical profile of a 30-year-old male patient with a history of betel nut chewing for the past 2 years, who exhibited sudden onset delusions, hallucinations, and disorganized speech and behavior upon increasing the dosage of betel nut consumption. The patient displayed a positive response to antipsychotic treatment, and symptoms resolved upon discontinuation of betel nut consumption. However, one month after discharge, the patient experienced a recurrence of auditory hallucinations upon resuming betel nut chewing. Through counseling and support, the importance of abstaining from betel nut use and maintaining medication compliance was emphasized, resulting in no recurrence of psychotic symptoms during the six-month follow-up.Conclusions: This case report highlights the related role of betel nut with brief psychotic disorder, especially when the chewing dosage is abruptly increased. It underscores the importance of considering betel nut as a potential precipitant related to acute psychiatric disorders in clinical settings.

Brief psychotic disorder related to areca nut use: a case report

BackgroundCatatonia presents itself as a complex neuropsychiatric syndrome, giving rise to various motor, speech, and behavioral challenges. It is noteworthy that approximately 10% of psychiatric hospital admissions can be attributed to this condition. It is imperative to note that cannabis-induced catatonia, while infrequent, has been linked to the use of marijuana. This connection has the potential to disrupt neurotransmitter systems, necessitating further research for a comprehensive understanding and effective treatment, particularly given the evolving trends in cannabis use. In this context, we shall delve into a unique case of recurrent cannabis-induced catatonia.</sec>Case presentationA 23-year-old gentleman, who has previously struggled with substance use disorder, experienced the emergence of mutism, social isolation, and a fixed gaze subsequent to his use of cannabis. Remarkably, despite the absence of hallucinations, he exhibited recurrent episodes of catatonia. These episodes were effectively addressed through a combination of electroconvulsive therapy (ECT) and lorazepam administration. Notably, when the lorazepam dosage was gradually reduced to below 2 mg per day, the catatonic symptoms resurfaced; however, they promptly abated upon reinstating the medication. The diagnosis of cannabis-induced catatonia was established, and its management primarily involved a therapeutic approach encompassing ECT and lorazepam. It is pertinent to underscore that this catatonic condition can be directly linked to the individual’s cannabis usage.</sec>ConclusionThe connection between cannabis and catatonia is intricate and not entirely comprehended. Although cannabis possesses therapeutic advantages, it can paradoxically trigger catatonia in certain individuals. Multiple factors, such as genetics, cannabinoids, and neurotransmitter systems, contribute to this intricacy, underscoring the necessity for additional research.</sec>

Background: Catatonia presents itself as a complex neuropsychiatric syndrome, giving rise to various motor, speech, and behavioral challenges. It is noteworthy that approximately 10% of psychiatric hospital admissions can be attributed to this condition. It is imperative to note that cannabis-induced catatonia, while infrequent, has been linked to the use of marijuana. This connection has the potential to disrupt neurotransmitter systems, necessitating further research for a comprehensive understanding and effective treatment, particularly given the evolving trends in cannabis use. In this context, we shall delve into a unique case of recurrent cannabis-induced catatonia.Case presentation: A 23-year-old gentleman, who has previously struggled with substance use disorder, experienced the emergence of mutism, social isolation, and a fixed gaze subsequent to his use of cannabis. Remarkably, despite the absence of hallucinations, he exhibited recurrent episodes of catatonia. These episodes were effectively addressed through a combination of electroconvulsive therapy (ECT) and lorazepam administration. Notably, when the lorazepam dosage was gradually reduced to below 2 mg per day, the catatonic symptoms resurfaced; however, they promptly abated upon reinstating the medication. The diagnosis of cannabis-induced catatonia was established, and its management primarily involved a therapeutic approach encompassing ECT and lorazepam. It is pertinent to underscore that this catatonic condition can be directly linked to the individual’s cannabis usage.Conclusion: The connection between cannabis and catatonia is intricate and not entirely comprehended. Although cannabis possesses therapeutic advantages, it can paradoxically trigger catatonia in certain individuals. Multiple factors, such as genetics, cannabinoids, and neurotransmitter systems, contribute to this intricacy, underscoring the necessity for additional research.

Recurrent cannabis-induced catatonia: a case report and comprehensive systematic literature review

Patients with comorbid neurological and psychiatric diseases often face considerable impairment, causing challenges that pervade many aspects of their lives. Symptoms can be especially taxing when one or more of these conditions is severely disabling, as the resulting disability can make it more challenging to address comorbidities. For clinicians, such patients can be quite difficult to both diagnose and treat given the immense potential for overlap between the underlying psychiatric and neurologic causes of their symptoms—as well as the degree to which they might exacerbate or, conversely, mask one another. These intricate relationships can also obscure the workup of more acute pathologies, such as alcohol withdrawal and delirium. This report details the complex history and clinical challenges in a 54-year-old man who was no longer able to work after developing multiple neurologic deficits from a left MCA stroke a decade earlier. The intellectual and motor disabilities he faced in the aftermath of his stroke were subsequently compounded by a steady increase in alcohol consumption, with his behavior ultimately progressing to severe alcohol use disorder. The coinciding neurologic and psychiatric manifestations obfuscate the workup—and therefore the management—of his major depressive disorder. In pursuit of the optimal approach to address these comorbid conditions and promote recovery, an investigation into possible mechanisms by which they are interconnected revealed several potential neuropsychiatric explanations that suggest targets for future therapeutic strategies.

Patients with comorbid neurological and psychiatric diseases often face considerable impairment, causing challenges that pervade many aspects of their lives. Symptoms can be especially taxing when one or more of these conditions is severely disabling, as the resulting disability can make it more challenging to address comorbidities. For clinicians, such patients can be quite difficult to both diagnose and treat given the immense potential for overlap between the underlying psychiatric and neurologic causes of their symptoms&#x2014;as well as the degree to which they might exacerbate or, conversely, mask one another. These intricate relationships can also obscure the workup of more acute pathologies, such as alcohol withdrawal and delirium. This report details the complex history and clinical challenges in a 54-year-old man who was no longer able to work after developing multiple neurologic deficits from a left MCA stroke a decade earlier. The intellectual and motor disabilities he faced in the aftermath of his stroke were subsequently compounded by a steady increase in alcohol consumption, with his behavior ultimately progressing to severe alcohol use disorder. The coinciding neurologic and psychiatric manifestations obfuscate the workup&#x2014;and therefore the management&#x2014;of his major depressive disorder. In pursuit of the optimal approach to address these comorbid conditions and promote recovery, an investigation into possible mechanisms by which they are interconnected revealed several potential neuropsychiatric explanations that suggest targets for future therapeutic strategies.

Case report: Diagnostic challenges in a patient with alcohol use disorder that developed following a stroke

Loperamide is an over-the-counter antidiarrheal for which increasing cases of abuse or misuse are described. We report the onset of opioid use disorder associated with low to moderate doses of loperamide in an intellectual disability patient without previous history of substance use disorder (SUD). Our patient presented strongly reduced activities of CYP3A and P-glycoprotein, which are mainly involved in loperamide metabolism and transport. We suggest that this led to an increase in bioavailability, systemic exposure, and brain penetration thus allowing loperamide to act on the central nervous system and contributing to the development of SUD. Slow release oral morphine (SROM) was chosen as opioid agonist treatment, which successfully contained loperamide use and globally improved her clinical condition. This situation highlights the need for caution and awareness when prescribing loperamide, particularly in vulnerable patients with few cognitive resources to understand the risks of self-medication and little insight into its effects.

Loperamide is an over-the-counter antidiarrheal for which increasing cases of abuse or misuse are described. We report the onset of opioid use disorder associated with low to moderate doses of loperamide in an intellectual disability patient without previous history of substance use disorder (SUD). Our patient presented strongly reduced activities of CYP3A and P-glycoprotein, which are mainly involved in loperamide metabolism and transport. We suggest that this led to an increase in bioavailability, systemic exposure, and brain penetration thus allowing loperamide to act on the central nervous system and contributing to the development of SUD. Slow release oral morphine (SROM) was chosen as opioid agonist treatment, which successfully contained loperamide use and globally improved her clinical condition. This situation highlights the need for caution and awareness when prescribing loperamide, particularly in vulnerable patients with few cognitive resources to understand the risks of self-medication and little insight into its effects.

Case Report: Opioid Use Disorder Associated With Low/Moderate Dose of Loperamide in an Intellectual Disability Patient With CYP3A and P-Glycoprotein Reduced Activity