Delayed identification and diagnosis of Huntington\u27s disease due to psychiatric symptoms

Huntington\u27s disease (HD) is a progressive neurodegenerative illness that affects 2-9/100.000 of the general population. The usual onset is at around age 35-40 years, but there were cases with onset above 55 years. The disease manifests clinically with many neurological and psychiatric symptoms, leading in advanced phases to dementia, but cognitive symptoms are frequently present much earlier in the disease course. HD is caused by an expanded polyglutamine stretch in the N-terminal part of a 350 kDa protein called huntingtin (HTT). This stretch is encoded by a trinucleotide CAG repetition in exon 1 of HTT. An expansion of greater than 36 repeats results in HD. The number of repeats is inversely correlated with the age of onset of motor symptoms, and disease onset during childhood or adolescence is associated with more than 60 CAG repeats. Mood disturbances may be one of the earliest symptoms of HD and may precede the onset of the motor pheno-type for almost 10 years. Neuropsychiatric symptoms may delay the appropriate diagnosis of HD and have major implications for disease management, prognosis and quality of life for patients and families. This case study is about a 58 years old female patient with late identification of Huntington\u27s disease after two admissions to psychiatric inpatient units, for the treatment of behavioral disturbances

ADMISSION TO THE PSYCHIATRIC EMERGENCY SERVICES OF PATIENTS WITH ALCOHOL-RELATED MENTAL DISORDER

Abstract

Sudden unexpected death in schizophrenia: Autopsy findings in psychiatric inpatients

Schizophrenia is associated with premature mortality and a high rate of sudden, unexpected deaths. Autopsy data are scant, and in studies using death certificates or root cause assessments, a majority of sudden deaths remained unexplained. In the community, post-mortem data indicate that the most common cause of sudden natural death is coronary artery disease. In this study, we used autopsy findings to determine the cause of sudden death in a consecutive cohort of 7189 schizophrenia patients admitted to a free-standing, psychiatric teaching hospital from 1989 to 2013. Medical record review identified 57 patients (0.79%) who died suddenly and unexpectedly during hospitalization. Autopsies were performed in 51 (89.5%) patients (55.9 +/- 9.4 years, male = 56.9%). Autopsy-based causes of sudden death were most commonly cardiovascular disorders (62.8%). Specific causes included myocardial infarction (52.9%), pneumonia (11.8%), airway obstruction (7.8%), myocarditis (5.9%), and dilated cardiomyopathy, hemopericardium, pulmonary embolus, hemorrhagic stroke and brain tumor (2.0% each). The sudden death remained unexplained in 6 (11.8%) patients, 3 of whom had evidence of coronary arteriosclerosis on autopsy. Patients with and without myocardial infarction were similar regarding age, gender, smoking, body mass index and psychotropic treatment (p values \u3e= 0.10). In conclusion, sudden cardiac death occurs at a 0.8% rate in a psychiatric hospital, well above general population rates. Autopsy findings indicate that sudden death in schizophrenia is caused by structural cardiovascular, respiratory and neurological abnormalities, with most cases due to acute myocardial infarction. Early recognition and treatment of coronary artery disease must become a clinical priority for all adults with schizophrenia. (C) 2014 Elsevier B.V. All rights reserved

Schizophrenia relapse after stopping olanzapine treatment during pregnancy: a case report

Women with schizophrenia have a high risk for symptom exacerbation or relapse during pregnancy and thereafter. Relapses are more frequent when antipsychotics are discontinued. This paper describes the case of a 28-year old woman with schizophrenia who continued treatment with olanzapine during the first trimester. Olanzapine, a second-generation antipsychotic, was administered at a therapeutic dose from week 1 of gestation until week 13 when she reported the pregnancy to her psychiatrist. Despite the psychiatrist\u27s recommendation to continue treatment, the patient stopped olanzapine at 20 weeks. She was hospitalized at week 36 for a schizophrenia relapse and was transferred to the obstetrics department where she gave birth by Cesarean section to a normal child. This case is important, illustrating the perils of unplanned pregnancy during antipsychotic treatment and abrupt discontinuation. Ultimately, clinical decisions should be made on a case-by-case basis, weighing the risks to the mother in terms of symptom exacerbation and relapse if antipsychotic treatment is discontinued, and the potential risk to the fetus regarding possible teratogenic effects of continued antipsychotic treatment

Switching bipolar disorder patients treated with clozapine to another antipsychotic medication: a mirror image study

Petru Ifteni,1,2 Andreea Teodorescu,1,2 Marius Alexandru Moga,1 Alina Mihaela Pascu,1 Roxana Steliana Miclaus1,2 1Faculty of Medicine, Transilvania University of Brasov, Brasov, Romania; 2Clinical Hospital of Psychiatry and Neurology Brasov, Brasov, Romania Abstract: Bipolar disorder (BD) is associated with periodic symptom exacerbations, leading to functional impairment, and increased risk of suicide. Although clozapine has never been approved for the treatment of BD, it is occasionally used in severe mania. The aim of the study is to evaluate the risks and benefits of switching clozapine in remitted BD patients. This is an observational, mirror image study of 62 consecutive remitted BD outpatients treated with clozapine. Twenty-five patients were switched to another antipsychotic following a change in a drug reimbursement rule, while 37 continued on clozapine. The mean time in remission was shorter for the switched group (9.2±4 months vs 13±6 months, P=0.018), and the number of patients who relapsed was larger (n=21 vs n=8, P<0.0001). The results suggest that switching from clozapine to another antipsychotic may increase the risk of relapses in remitted patients with BD. Keywords: clozapine, bipolar disorder, relapse, switch, cos

Rapid clozapine titration in treatment-refractory bipolar disorder

Background: Clozapine is effective in treatment-refractory bipolar disorder (BD). Guidelines recommend slow titration to prevent seizures, hypotension and myocarditis, but this stance is not supported by comparative data. Objective: To evaluate the safety and effectiveness of rapid clozapine titration in BD. Methods: Analysis of a consecutive cohort of treatment-refractory BD patients with mixed/manic episode admitted on alternate days to one of two units of a psychiatric hospital. On one unit, clozapine was started at 25 mg followed by 25-50 mg as needed every 6 h (maximum 100 mg/day) on clay 1, followed by increases of 25-100 mg/day. On the other unit, clozapine was initiated with 25 mg in day 1, followed by increases of 25-50 mg/day. The primary outcome was the number of days from starting clozapine until readiness for discharge, adjusted in logistic regression for the number of antipsychotics tried during the hospitalization, psychotropic co-treatments and presence of psychotic features. Results: Patients subject to rapid (N = 44) and standard (N = 23) titration were similar in age, gender, smoking status, body mass index, illness severity at baseline and discharge, and highest clozapine dose. Clozapine was discontinued due to hypotension (N = 1) and pneumonia (N = 1) during rapid titration, and for excessive sedation (N = 1) in each titration group. The number of hospital days from starting clozapine until readiness for discharge was 3.8 days shorter in the rapid titration group (12.7 +/- 6.3 vs. 16.5 +/- 5.8, p = 0.0077). Conclusion: Rapid clozapine titration appeared safe and effective for treatment-refractory BD. The potential for shorter hospital stays justifies prospective trials of this method. (C) 2014 Elsevier B.V. All rights reserved

Effectiveness and safety of rapid clozapine titration in schizophrenia

Objective: Clinical guidelines recommend slow clozapine dose titration in order to decrease the risk of seizures and hypotension. The recommendation may delay adequate control of severe psychotic symptoms. We evaluated the safety and effectiveness of rapid clozapine titration in patients who had been previously exposed to the drug and in patients who received clozapine for the first time after failing to respond to other antipsychotics. Method: Analysis of hospital course of a consecutive cohort of schizophrenia patients (N = 111) who received 25-100 mg of clozapine as needed every 6 h the first treatment day, followed by upward adjustments of 25-100 mg/day. Results: Symptom control was obtained with an average dose of 353 +/- 174 mg/day after 4.1 +/- 3.1 days in the 73 patients previously treated with clozapine. For the 38 patients initially started on other antipsychotics, the average clozapine dose required for symptom control (409 +/- 188 mg/day) was reached after 7.1 +/- 4.8 days. None of the patients had seizures, severe hypotension or other major adverse reactions. Conclusion: In this naturalistic cohort study rapid clozapine titration appeared safe and effective for the treatment of schizophrenia. The results justify controlled clinical trials of this treatment method