Psychiatry research case reports最新文献

Background

Case presentation

Discussion

High levels of cannabis use have been established as a risk factor for the development of psychotic disorders and may exacerbate existing mental illness. Despite extensive research on the adverse effects of cannabis, less attention has been given to a concerning phenomenon: the onset and exacerbation of acute psychotic symptoms following abrupt cessation of cannabis use. This case series presents three individuals who developed their first episode of psychosis shortly after discontinuing heavy cannabis use (several grams daily). These cases underscore the potential link between cannabis withdrawal and the emergence or exacerbation of psychotic symptoms which may led to a psychotic episode, highlighting the need for greater public health awareness of safe cannabis use practices. The discussion explores potential mechanisms such as dysregulation of the endocannabinoid and dopamine systems following long-term cannabis use, which may predispose individuals to psychosis during withdrawal. The findings advocate for safer cannabis discontinuation guidelines, suggesting gradual reduction in cannabis use and potency of product consumed as preventive measures. Further research is essential to explore predictive risk factors and refine approaches to mitigate the risk of psychosis associated with cannabis withdrawal in vulnerable populations.

Clozapine is an atypical antipsychotic agent often recommended after the failure of two or more antipsychotics for treatment-resistant schizophrenia. Clozapine has proven efficacy in reducing morbidity and suicide in schizophrenic patients. However, it is generally underutilized for eligible patients, primarily because of the associated side effects. Notably, clozapine's side effects on the gut include hypomotility, constipation, and dysphagia, which are secondary to the anticholinergic properties of the medication. Thus far, there remains a dearth in the literature regarding reported foreign body sensations on the throat. Therefore, we report a case of foreign body sensation on the throat in a patient receiving clozapine. Foreign body sensation on the throat is an alarming concern, given the role of the oropharynx in the airway. Hence, it is imperative to evaluate unfamiliar body sensation on the throat as part of comprehensive assessment of the gut side effects of clozapine therapy.

Déjà vu experiences in dementia are notably underreported and remain an area of limited research within the literature. Despite the prevalence of dementia, the phenomenon of déjà vu has received relatively little attention in clinical settings. Consequently, healthcare workers may overlook this symptom, potentially leading to delayed diagnosis and management of dementia-related issues. Our manuscript addresses this gap by presenting a case study of déjà vu experiences in a patient with dementia. By documenting and analysing such occurrences, we aim to raise awareness among healthcare professionals about the diverse symptoms that may manifest in dementia, including those less commonly recognised. Future studies investigating the prevalence, mechanisms, and clinical implications of déjà vu in dementia patients are warranted to deepen our understanding and improve the quality of care provided to individuals affected by this debilitating condition.

Background

Drug-induced Liver Injury (DILI) is a common cause of acute liver injury and can be induced by several drugs. Lamotrigine, an antiepileptic drug, and quetiapine are used also as mood stabilizer medications and both have been reported to induce liver toxicity. The prescription of lamotrigine in association with other antidepressants can occur frequently in clinical practice, especially when depressive symptoms are resistant to monotherapy or are long-standing. The case we report highlights the likelihood of DILI with secondary liver damage due to the association between lamotrigine, quetiapine and sertraline through dose-dependent and not immune-mediated mechanisms.

Case presentation

We present the case of a young adult female with recurrent major depression that, after dose remodulation of antidepressant therapy with lamotrigine, quetiapine and sertraline, experienced abdominal pain with evidence of acute liver injury. Liver damage went into remission after antidepressant therapy was discontinued. DILI appears as a probable explanation for these findings (6 points in items for hepatocellular injury in the updated RUCAM score) caused by the interaction between these drugs.

Conclusions

This harmful effect is not yet well documented in the literature, and it seems to be due to a non-immune dose-dependent toxic effect. Caution is therefore warranted when prescribing the association of lamotrigine, quetiapine and sertraline.

Patients with severe mental illness (SMI) are ∼3 times more likely to live with obesity and experience a 2 - 3 fold higher mortality rate from cardiovascular disease compared to the non-psychiatric general population. Antipsychotic drugs (APDs), though effective in ameliorating symptoms of SMI, directly contribute to adverse metabolic effects including weight gain. Counteracting antipsychotic induced weight gain (AIWG) with pharmacological strategies and lifestyle modifications has demonstrated limited effects in previous studies. The use of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) has recently become widespread in medicine. GLP-1 RAs offer a relatively novel and potentially effective approach to counteract weight gain and improve cardiometabolic abnormalities associated with commonly prescribed APDs in individuals with SMI.

In this retrospective case series, two chronic state mental health hospital patients living with obesity in the context of past medical issues and currently receiving clozapine, an APD with high metabolic risks, had also been receiving dulaglutide (supplemented with diet and weight management counsel) as an off-label intervention to promote weight loss. Retrospective review of patient data revealed encouraging results on weight and glyco-metabolic parameters in each of the two cases. In particular, in weight, Patient 1 achieved a 22 % reduction and Patient 2 achieved a 16 % reduction. In HbA1c levels, both patients achieved a 5 % reduction. In triglyceride levels, Patient 1 achieved a 46 % reduction and Patient 2 achieved a 68 % reduction. These results provide a compelling argument for the adoption of GLP-1 RAs in treatment plans for such oft-forgotten and stigmatized state mental health hospital patients, who often: have chronic lengths of stay, are on clozapine and/or polypharmacy medication regimens, are sedentary, and have AIWG, metabolic syndrome, or other significant comorbidities.

Background

While clozapine withdrawal side effects have been documented, few case reports have described its potential to cause withdrawal catatonia. Here, we present a case of a patient with schizophrenia who developed catatonia within seven days of clozapine discontinuation.

Case presentation

A 47-year-old male, with a history of schizophrenia on clozapine 600 mg daily, initially self-presented to the clinic for change in regimen, and was admitted to inpatient psychiatry due to disorganized thoughts. After a coincidental finding of urosepsis, he was transferred to the medical service for antibiotic treatment during which time clozapine was restarted. While infection improved, the patient became progressively less interactive and by day 7 was diagnosed with catatonia. Intramuscular lorazepam was trialed but led to oxygen desaturation requiring brief ICU monitoring, and resulted only in temporary improvement. Furthermore, patient displayed intermittent autonomic instability, concerning for malignant catatonia. He was ultimately transferred to another hospital for electroconvulsive therapy (ECT). Patient gradually returned to psychiatric baseline after 5 ECT sessions, re-titration of clozapine back to home dose, with short course of lorazepam as adjunctive therapy.

Conclusion

This case adds to existing evidence that clozapine discontinuation may induce catatonia. The current theory of the underlying mechanism involves clozapine's action at the GABAergic system through direct and indirect mechanisms and receptor changes with chronic clozapine use. Understanding this phenomenon helps inform decision-making with clozapine initiation and discontinuation and suggests potential treatment guidelines for catatonia in the context of clozapine withdrawal.

Background

Corpus callosum agenesis (ACC) is a rare congenital condition that presents heterogeneously. Growing data have showcased incidental findings of ACC following neuropsychiatric presentations.

Case presentation

A widow in her sixties presented with an episode of self-harm. The event occurred during a depressive episode with psychotic symptoms and was precipitated by bereavement. Leading up to the presentation and weeks thereafter, family and acute mental health unit staff reported abnormal behaviours, social isolation, urinary incontinence, and self-neglect. General systemic and neurological examination was within normal limits. Cognitive examination revealed deficits primarily in executive function, fluency, and visuospatial function. Magnetic Resonance Imaging of the brain revealed complete corpus callosum agenesis. After inpatient multidisciplinary treatment, her depressive and psychotic symptoms resolved, and the patient returned to premorbid functioning.

Conclusion

The implication of corpus callosum agenesis in the development and manifestation of neuropsychiatric manifestations is discussed following literature review.