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.

A new measurement protocol to differentiate sources of halitosis.

OBJECTIVE: Three sources of halitosis exist, potentially in any combination: mouth, nasal cavity or alveolar breath. There has been no universally accepted protocol which differentiates and quantifies each odour source separately. In this study a new gas measurement protocol is described and tested to determine whether each odour source can be separately detected without contamination. MATERIALS AND METHODS: Ninety healthy volunteers were divided into three groups. Hydrogen sulphide (H2S), volatile organic compounds (VOCs) and hydrogen (H2) were artificially generated in the mouth, nose and pulmonary alveoli, respectively. VOC, ammonia (NH3), sulphur dioxide (SO2), H2S and H2 gas readings from mouth, nose and alveolar air were measured and compared. Measurements were taken before and during gas generation. RESULTS: Contamination of nasal air (2.8%) and alveolar air (5.0%) by oral H2S; alveolar air (2.06%) and oral air (4%) by nasal organic gas; nasal air (18.43%) and oral air (9.42%) by alveolar H2 was calculated. CONCLUSION: The results demonstrated that artificially generated oral H2S nasal VOC and alveolar H2 can be individually quantified. This gas measurement protocol can be used diagnostically or to gauge response to therapy in any medical or dental setting.

Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment.

BACKGROUND: There has been much evidence in recent years that free oxygen radicals and nitric oxide (NO) may play an important role in the pathophysiology of neuropsychiatric disorders. In this study, we aimed to investigate whether NO, xanthine oxidase (XO), superoxide dismutase (SOD), and adenosine deaminase (ADA) levels are associated with major depression (MD) and to evaluate the impact of antidepressant treatments on NO, SOD, ADA and XO levels in MD. METHODS: Thirty-six patients who were diagnosed as MD according to DSM-IV criteria and 20 healthy controls were included. The serum levels of NO, XO, SOD, and ADA were measured by spectrophotometric methods both in patients and controls. Patients were treated with antidepressant drugs for 8 weeks. All patients were assessed by Hamilton Depression Rating Scale (HDRS) both before and after antidepressant treatment. RESULTS: ADA and XO levels of the patients were significantly higher than the controls. SOD level of the patients was significantly lower than the controls. Although NO levels of the patients were higher than the controls, the difference was not statistically significant. There was no correlation between HDRS and the parameters studied (SOD, ADA, XO, and NO) of the patients. After 8 weeks of antidepressant treatment, ADA and SOD activities were increased, whereas NO and, XO levels decreased significantly. CONCLUSIONS: ADA, XO, and SOD activity may have a pathophysiological role in MD and may predict prognosis of MD. Activity of these enzymes may be used to monitor effects of the antidepressant treatment.

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.

Diagnostic Value of Halitosis Examination Methods.

There are many methods and varied protocols for examining halitosis. Chemical and enzymatic tests determine the presence of bacterial species and their metabolic products or enzymes in the mouth, while halitometers precisely quantify gases but not halitosis itself. Examinations by the human nose (ie, self assessment, feedback from others, or organoleptic test by an examiner) directly target halitosis, however organoleptic examination alone is insufficient for a definitive diagnosis when the individual has no complaints about halitosis. The underlying reasons why patients seek consultation concerning halitosis are usually based on their own assessment and the opinion of others, even if those assessments are not correlated with oral odorous gas measurements. This article seeks to summarize findings and review methods of examining halitosis to determine their usefulness.

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.

Possible role of nitric oxide and adrenomedullin in bipolar affective disorder.

Nitric oxide (NO) has been implicated to play a role in the pathogenesis of depressive disorders. 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. Therefore, it is suggested that these two molecules may play a role together in the brain. We aimed to examine AM and NO in bipolar affective disorder (BPAD). Forty-four patients with BPAD and 21 healthy control subjects were included in this study. DSM-IV diagnosis of bipolar affective disorder (type I, manic episodes) was independently established by two psychiatrists and the Turkish version of the Bech-Rafaelson Mania Scale was administered. Also, a semistructured form was used to ascertain several sociodemographic and clinical variables of the patients. AM and NO were studied in plasma. The mean value of plasma NO levels in the BPAD group of 46.58 +/- 13.97 micromol/l was significantly higher than that of controls (31.81 +/- 8.14 micromol/l) (z = -4.15, p = 0.000). Mean plasma AM levels were found to be increased in patients with BPAD (35.13 +/- 5.26 pmol/l) compared to controls (16.22 +/- 3.02 pmol/l) (z = -6.16, p = 0.000). AM levels of BPAD patients were approximately 2-fold higher than controls. AM levels were positively correlated with the duration of hospitalization for the current episode and negatively correlated with the total duration of illness. Both NO and AM may have a pathophysiological role in BPAD (type I, manic episodes) and the clinical symptomatology and prognosis of BPAD.