Psychiatry research case reports最新文献

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.

Treatment resistant depression (TRD) is a term used to define a failure of treatment, despite having two or more adequate trials of antidepressant medication. Our case study focuses on the struggles to achieve sustainable remission in a young adult female and how the condition impacted her overall quality of life. The patient underwent numerous interventions including use of different classes of antidepressant medications, mood stabilizers, therapy, and ECT (electroconvulsive therapy) before she found sustainable improvement with biweekly IV ketamine infusions along with oral pramipexole. Although there are multiple pathways that lead to depression, we hypothesize that this combination may have addressed a state of ‘dopamine deficiency’ in the mesolimbic dopaminergic pathway that led to improvement in the patient's depressive symptoms. In addition, the paper also attempts to rationalize these findings based on a preclinical study done on mice undergoing forced swim tests (FST), that shows the synergistic effects on D2/3 receptors by combining these two drugs.

Contingency management (CM) is an effective behavioural treatment for substance use disorder (SUD) that involves providing incentives (e.g., vouchers) for target behaviours related to recovery. Despite evidence of its efficacy with SUD, little is known about its feasibility for the treatment of other addictive disorders. Here, we sought to investigate the feasibility of a remote-delivered CM intervention in promoting gambling treatment-related outcomes. Voucher-based incentives were provided contingent on abstinence from gambling, attendance at treatment, and completion of weekly recovery-related goals. Overall, the present findings indicate that CM procedures can be feasibly and advantageously applied as an adjunct treatment to promote recovery from harmful gambling. Further research is needed on larger-scale evaluations and methods of disseminating the wider adoption of CM for the treatment of harmful gambling.

Fibromyalgia is a neurological condition caused by glutamate dysregulation which leads to central sensitization. It is characterized by chronic widespread pain, fatigue, headache/migraine, sleep issues, and cognitive dysfunction, and is commonly comorbid with gastrointestinal symptoms, depression, and anxiety. Due to a lack of widespread effective treatment options, many patients are seeking out cannabis as a treatment, though little is known about the contraindications for its use.

This case study presents information on a non-Hispanic 27-year-old African American woman with fibromyalgia and schizoaffective disorder who was using cannabis as a treatment for her pain. She was put on the low glutamate diet to treat her fibromyalgia, which significantly reduced her pain and other symptoms after one month, allowing her to discontinue the use of the cannabis. This discontinuation in turn drastically reduced her psychiatric symptoms. Her case is presented along with a discussion on the glutamatergic mechanisms which may be responsible for this effect, known side effects of cannabis, and potential contraindications for its use.

This case study demonstrates that while cannabis may have pain relieving properties, it can also increase the likelihood of psychosis. In this case study, there was no safe daily dosage of cannabis noted. After experiencing symptom relief from the low glutamate diet, the patient discontinued the use of cannabis which led to further psychiatric improvements. The literature suggests that this adverse effect appears to be mediated by glutamate and may be more pronounced with early age of use, increasing dosage, high potency, and in those who may be predisposed to psychiatric illness. Physicians should inquire about self-treatment with cannabis in individuals being treated for pain who present with comorbid psychiatric illness, especially psychotic symptoms.

Multiple authors have discussed challenges in diagnosis and management of catatonia, but there are limited case studies highlighting multiple issues in both domains concurrently. We present a case of first-episode akinetic catatonia in a 63-year-old male with a history of treatment-resistant depression, to highlight multiple diagnostic and therapeutic challenges in catatonia and discuss learning points. The patient had a likely episode of transient ischemic attack (TIA) which precipitated delirium, and subsequently developed catatonia and severe hyponatremia. The cause behind his acute catatonia was unclear. Catatonic symptoms did not improve with benzodiazepines, while side effects of oversedation and ongoing delirium limited further uptitration of benzodiazepines. Electroconvulsive therapy was also not initiated in view of vascular risks with the recent TIA. The patient's catatonia subsequently resolved spontaneously with treatment of his medical conditions. This case highlights the complexity behind identifying etiologies of catatonia with the interplay of multiple medical conditions on the background of an affective disorder and ongoing delirium. It also illustrates therapeutic challenges in the context of unresponsiveness to benzodiazepines, presence of concomitant delirium and contraindications to initiating electroconvulsive therapy. We discuss learning points in reference to latest guidelines in management of catatonia by the British Association of Psychopharmacology (BAP), and review related literature. We discuss etiologies of catatonia, the relationship between catatonia and delirium, and offer recommendations in the face of therapeutic challenges discussed. There is a need for further research and clarification of guidelines in regard to contraindications to ECT and management of catatonia with ongoing delirium.

Psychogenic polydipsia (PPD) is a condition characterized by excessive water intake that is not related to a physiological need. It is often seen in patients with schizophrenia and schizoaffective disorders and can lead to hyponatremia, a serious condition characterized by low sodium levels in the blood. This report summarizes the case of a 74-year-old male who had a longstanding history of schizoaffective disorder, bipolar type. At admission to the geriatric unit of a psychiatric hospital, the patient engaged in excessive drinking behavior and his serum sodium level was low (126 mmol/L). The patient required urgent treatment, however had a history of ineffective medication trials (including clozapine), and poor medication adherence. As such, the patient's family member who was the substitute decision maker consented to electroconvulsive therapy (ECT). Upon beginning ECT, there was noted improvement in PPD symptoms with regards to water seeking and eventually improved oral compliance for mediations. The patient completed 25 sessions of ECT and was discharged three months after admission. Significant improvements were also noted in symptoms of psychosis between admission and discharge. Overall, this case report offers ECT as a potential treatment modality for geriatric patients presenting with symptoms of PPD with psychosis.

Pulsatile tinnitus (PT) is a rare form of tinnitus affecting 3–5 million Americans characterized by the perception of a rhythmic sound. Diagnosing PT in the clinical setting is important, as it is commonly caused by underlying vascular pathologies (i.e., arteriopathies or venopathies) leading to an increased risk of stroke, blindness, or deafness, though identifying it presents a challenge due to the broad depiction of PT's distinguishing auditory perception (Narsinh et al., 2022). As such, atypical presentations of PT may be misdiagnosed as other neurologic or psychiatric disorders. Here, we present a case where pulsatile tinnitus took the form of debilitating auditory hallucinations ultimately requiring inpatient psychiatric hospitalization, demonstrating the importance of a thorough evaluation and multidisciplinary consultation in the workup and long-term care for these patients.

The connection between COVID-19 infection and psychosis is an evolving topic of discussion. Physicians are still trying to understand how COVID-19 can lead to, influence, and impact a diagnosis of psychosis—an inherently complicated diagnosis with various etiologies. This case report describes the clinical course of a 25-year-old male who presented to the emergency department with an acute onset of paranoia, visual hallucinations, and delusions of unknown durations after testing positive for COVID-19 2 weeks prior to admission. He was admitted to the neurology critical care unit, neurological causes of his psychosis were ruled out, and psychiatry was consulted. Initial risperidone administration resulted in symptoms of hyperactive catatonia which was then treated with a lorazepam challenge showing moderate improvement of irregular motor activity but continued agitation and hallucinations. Despite the diagnosis of catatonia, delirium precautions were still taken, such as maintaining day/night cycles, frequent reorientation, minimizing restraints, and verbal redirection. First haloperidol, then switched to chlorpromazine, improved his disposition and communication, but hallucinations and delusions persisted throughout the duration of his stay. Of note, a nucleic acid amplification test was positive for active COVID-19 infection on hospital day 5, and negative on subsequent testing. Psychiatry's final impression was “schizophreniform including possible contributing residual delirium from COVID-19 or other causes” due to symptoms persisting for more than a month, positive hallucinations and delusions, a catatonic state, and negative symptoms. This case report captures the difficulty of determining the etiology of psychosis when complicated by concurrent COVID-19 infection. It is unclear how COVID-19 impacted the diagnosis and disease course. Delirium has not been shown to be a common feature of COVID-19 infection, but acute stressors have been shown to lead to the onset of schizophrenic psychosis in genetically susceptible individuals. Further research is needed to further understand the relationship between COVID-19, delirium, and schizophrenia, and any case of altered mental status, especially when complicated by COVID-19, merits a comprehensive history and workup to fully appreciate the interaction between various disease states.

COronaVIrus Disease 19 (COVID-19) has led to a global health crisis and dramatically changed people's lifestyles. Several neuropsychiatric complications, including catatonia, have been reported as either para- or post-infectious complications of COVID-19. We describe three cases of catatonia associated with COVID-19, presenting with distinct psychiatric histories and medical contexts.

Putative pathogenic mechanisms of COVID-19-related catatonia involve a combination of direct viral neuronal damage and neuroinflammation secondary to cytokine storm. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) can reach the central nervous system via axonal transport along sensory nerves or via haematogenous spread. The pathogenic pathways activated by viral infection may also affect neurotransmission in basal ganglia involving gamma-aminobutyric acid, dopamine, and glutamate systems. In some cases, COVID-19 can lead to anti-NMDA receptor encephalitis by activating mechanisms of molecular mimicry.

These cases highlight the importance of appropriate screening of neuropsychiatric manifestations after COVID-19 infection and early diagnosis of catatonia. Therapeutic strategies include the use of benzodiazepines and electroconvulsive therapy as first-line treatments for catatonia, despite some concerns related to poor response or medical complications of COVID-19 infections. Mounting evidence suggests that augmentation with a NMDA receptor antagonist is a useful therapeutic option, especially for treatment-resistant catatonia.