Murat Eren Ozen

The possible pathophysiological role of plasma nitric oxide and adrenomedullin in schizophrenia

Evidence is accumulating for a possible role of nitric oxide (NO) in schizophrenia. Adrenomedullin (AM) induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of NO. AM immune reactivity is present in the brain consistent with a role as neurotransmitter. We aimed to examine plasma levels of nitrite (a metabolite of NO) and AM in schizophrenic patients. Eighty-two patients with schizophrenia and 21 healthy control subjects were included in this study. DSM-IV diagnosis of chronic schizophrenia was established on the basis of independent structured clinical interviews and review of records by two qualified psychiatrists which included the Brief Psychiatric Rating Scale (BPRS), The Scale for the Assessment of Negative Symptoms (SANS) and The Scale for the Assessment of Positive Symptoms (SAPS). Total nitrite and AM have been studied in plasma. The mean values of plasma nitrite and AM levels in schizophrenic group were significantly higher than control values, respectively (P=0.03, P<0.0001). AM levels of schizophrenic patients were three fold higher than controls. In correlation analyses, there were statistically significant positive correlations between AM level and SAPS-delusion subscale (r=0.27, P=0.04); SAPS-bizarre behavior subscale (r=0.28, P=0.03) and SAPS-total (r=0.36, P=0.005). There is no correlation between total nitrite and AM levels (r=0.11, P=0.31). Both NO and AM may have a pathophysiological role in schizophrenia, and clinically symptomatology and prognosis of schizophrenia. This subject needs further study including treatment response and subtypes of schizophrenia.

Quetiapine and Ziprasidone as Adjuncts in Treatment-Resistant Obsessive-Compulsive Disorder : A Retrospective Comparative Study

Background and objective:While serotonin reuptake inhibitors (SRIs) are first-line pharmacological agents in the treatment of obsessive-compulsive disorder (OCD), 40–60% of patients with the disorder do not respond to these agents. This suggests that other neurotransmitters may play a role in OCD. In this regard, there has been particular interest in the dopaminergic system, with various antipsychotic drugs having been used as adjunctive therapy for refractory OCD. The aim of this study was to compare the efficacy of quetiapine and ziprasidone as adjuncts for treatment-resistant OCD.Methods:A total of 24 OCD patients treated with either quetiapine (n = 15) or ziprasidone (n = 9) as adjunctive therapy to high-dose SRI treatment were included in this retrospective evaluation. Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and Clinical Global Impression (CGI) scale scores were used to evaluate baseline clinical status and clinical improvement at 1, 2, 3 and 6 months of follow-up.Results:Clinical improvement was established in 80% of the quetiapine group and in 44.4% of the ziprasidone group with an overall mean improvement rate on the Y-BOCS scale of 66.7%. Both Y-BOCS and CGI mean scores were higher in the ziprasidone group at 2, 3 and 6 months follow-up than in the quetiapine group.Conclusions:In the first reported study of its role in this setting, ziprasidone was found to be less effective than quetiapine in the treatment of refractory OCD.

Neuroleptic malignant syndrome induced by ziprasidone on the second day of treatment

Neuroleptic malignant syndrome (NMS) is the rarest and most serious of the neuroleptic-induced movement disorders. We describe a case of neuroleptic malignant syndrome (NMS) associated with the use of ziprasidone. Although conventional neuroleptics are more frequently associated with NMS, atypical antipsychotic drugs like ziprasidone may also be a cause. The patient is a 24-year-old male with a history of schizophrenia who developed signs and symptoms of NMS after 2 days of treatment with an 80-mg/day dose of orally administrated ziprasidone. This case is the earliest (second day of treatment) NMS due to ziprasidone reported in the literature.

Can the retinal ganglion cell layer (GCL) volume be a new marker to detect neurodegeneration in bipolar disorder

PURPOSE The aim of this study was to compare the ganglion cell layer (GCL) volume and retinal nerve fiber layer (RNFL) thickness in bipolar patients and controls using optic coherence tomography to demonstrate neurodegeneration in bipolar disorder. METHODS This study involved 43 euthymic bipolar I patients who were being followed by the Psychiatry Department of Adiyaman University Medical School and 43 healthy volunteers as controls. Optic coherence tomography (OCT) measurements were performed for both groups. The RNFL thickness and GCL volumes were measured and recorded automatically by a spectral OCT device. FINDINGS No differences in sociodemographics were detected between groups, except for unemployment status, which was significantly higher in the patient group. The RNFL thickness was lower in patients compared with controls at all measured regions, and this decrease was statistically significant for the global RNFL measurement. The GCL volume was also significantly lower in the patient group. There was a significant negative correlation between the disease parameters, such as the disease duration, YMRS score, CGI score, and number of hospitalizations, and GCL volume. DISCUSSION These findings suggest that neurodegeneration occurs during the course of bipolar disorder. This degeneration may be demonstrated by decreased GCL at early stages, and as the disease progresses, involvement of other retinal layers, such as the RNFL and IPL, may be observed.

Neuroleptic malignant syndrome induced by ziprasidone on the second day of treatment: A case report

Dear Editor, This article is in reply to ‘‘Comments on the report of neuroleptic malignant syndrome induced by ziprasidone’’ by Branimir Margetić and Branka Aukst-Margetić (Margetić and Aukst-Margetić 2007), and we answer their queries on our case report. We took the patient under custody with the help of our service crew to prevent harm to ourselves or the patient, and to prevent a suicide attempt. We carried out regular visits. Administration of only a single dose of ziprasidone was documented. We noted that no other psychotropic drug was used. It was carefully observed that the patient had not taken any other antipsychotic drugs, including ziprasidone. On examination during the period after discharge, the patient still had psychotic signs, so we decided to prescribe another atypical antipsychotic for maintenance. Olanzapine was administered on the 10th day after discharge (the 20th day from application). We followed-up the patient 3 months after discharge on olanzapine treatment. In the follow-up, the patient was called for visits twice a week, accompanied by family members. We documented the illness history with the help of family members. There was no mood component in the course of the illness. In fact, many lethal catatonic states include a mood component; most cases give a history of depression with psychotic features or bipolar disorder. Lethal catatonia and malign hyperthermia included in hyperthermic syndromes related to medication were excluded because of diaphoresis, muscle rigidity, elevated CK, leukocytosis and history of antipsychotic use (Kaplan and Sadocks 2003). Although both lethal catatonia and neuroleptic malignant syndrome (NMS) have similar signs or symptoms, discontinuation of the antipsychotic drug usually results in resolution of NMS. The important clue for settling on a diagnosis was that the patient had never been administered an antipsychotic medication until the application of ziprasidone. The use of diazepam and biperiden was the simplest and most effective way of administration in an emergency situation, so that no time was lost in beginning the treatment. There are several publications which show the use of biperidene in NMS treatment (Unal et al. 1996; Hasan et al. 1999; Yumru et al. 2006). We began treatment with daily administration of intravenous diazepam (15 mg/day) and biperiden (15 mg/day) after the diagnosis was made. Doses were the same until the day of discharge. Gradual decrements, 5 mg/day decreased for a week, were planned. Diazepam and biperiden were given orally from discharge onwards, and by the third week, 14 days later, the administration of these agents was stopped. The gradual resolution of NMS symptoms was well documented, ending on the 10th day. The ESRS Parkinsonism subscale score was 28 on the first day of admission. By the 11th day after admission, the ESRS parkinsonism subscale score decreased to 0, and the patient was discharged.

Improvement of an atypical Kikuchi-Fujimoto disease (KFD) with antidepressant treatment: the first psychiatric approach to a KFD case

ABSTRACT Kikuchi-Fujimoto disease (KFD) is a sporadic and benign disorder of the lymph nodes of young individuals. A preceding fever, occasional skin rashes, and lymphopenia, suggest a viral aetiology and there have been reports of viral association. However, so far, no infectious agent has been proved to be aetiologically related. We herein report KFD in a 27-year-old female who presented with fevers, weight loss and tender cervical lymph nodes. The patient had depressive symptoms before the onset of KFD. During the disease process, depressive symptoms worsened with the KFD course. She had not relieved with the supportive treatment and major depressive disorder (MDD) became more severe gradually. After the treatment of MDD and with the improvement of mental health, clinical symptoms and the lymph node growth became reversed. The authors conclude that this clinical course of KFD with the treatment of MDD suggests an immune system response or immunological problem in these patients.

Massive uvula oedema during lithium therapy and resolution after lithium discontinuation

Acute oedema of the uvula is relatively rare, and often idiopathic. There are only a few cases reported up to date. This is the first case of oedema in the uvula that occurred during lithium treatment of a patient with bipolar-I manic disorder.