The Effect of Risperidone on Metabolite Measures in the Frontal Lobe, Temporal Lobe, and Thalamus in Schizophrenic Patients. A Proton Magnetic Resonance Spectroscopy ( 1 H MRS) Study

Department of Psychiatry, Medical University in Bialystok, Bialystok, Poland.
Pharmacopsychiatry (Impact Factor: 1.85). 10/2005; 38(5):214-9. DOI: 10.1055/s-2005-873156
Source: PubMed


The aim of the study was the evaluation of risperidone effect on metabolite measures in the frontal lobe, temporal lobe and thalamus in schizophrenic patients on the basis of proton magnetic resonance spectroscopy ( (1)H MRS).
A group of 14 patients with the diagnosis of schizophrenia, according to DSM-IV, were examined in the study. The patients were examined twice, once after a period of at least 7 days without neuroleptics and for the second time at least 4 weeks after stable risperidone doses.
The significant differences in the metabolite levels before and after the treatment were observed only in thalamus: an increase in myoinositol (mI) and N-acetylaspartate (NAA) levels. Positive symptoms before the treatment correlated positively with NAA level in the frontal lobes and negatively in the temporal lobes. Negative symptoms before the treatment correlated positively with Glx (a common signal for GABA, glutamine and glutamate) level in the temporal lobes.
Our results seem to confirm the influence of risperidone on the brain metabolism, specifically in the region of thalamus.

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    • "Several studies investigated the possible relationships between glutamatergic levels in the thalamus and clinical/behavioral symptoms as measured by the SANS and SAPS (Theberge et al., 2002, 2007; Bustillo et al., 2010; Aoyama et al., 2011), PANSS (Szulc et al., 2005, 2011, 2012; Yoo et al., 2009) and GAF scale (Egerton et al., 2012). No significant correlations were reported. "
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    ABSTRACT: The last fifteen years have seen a great increase in our understanding of the role of glutamate in schizophrenia (SCZ). The glutamate hypothesis focuses on disturbances in brain glutamatergic pathways and impairment in signaling at glutamate receptors. Proton Magnetic Resonance Spectroscopy ((1)H-MRS) is an MR-based technique that affords investigators the ability to study glutamate function by measuring in vivo glutamatergic indices in the brains of individuals with SCZ. (1)H-MRS studies have been performed comparing glutamatergic levels of individuals with SCZ and healthy control subjects or studying the effect of antipsychotic medications on glutamatergic levels. In this article we summarize the results of these studies by brain region. We will review the contribution of (1)H-MRS studies to our knowledge about glutamatergic abnormalities in the brains of individuals with SCZ and discuss the implications for future research and clinical care.
    Schizophrenia Research 01/2014; 152(2-3). DOI:10.1016/j.schres.2013.12.013 · 3.92 Impact Factor
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    • "According to our previous report, after at least 7 days without neuroleptic medication, a positive symptoms score correlated positively with NAA level in the frontal lobe and negatively with NAA level in the temporal lobe [7]. Another report from our facility showed the following positive correlations: negative PANSS, general scale, total scale and choline level in the thalamus (on left side) in the group of patients in the course of neuroleptic therapy (chronic patients and first-episode patients) [9]. "
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    ABSTRACT: Proton magnetic resonance spectroscopy (1H MRS) allows for examining brain functions in vivo in schizophrenic patients. Correlations between N-acetylaspartate (NAA) level in the frontal lobe and cognitive functions and clinical symptoms have been observed. The aim of the present study was evaluation of relationship between clinical symptoms, cognitive outcomes and brain function in 1H MRS measures in schizophrenic patients. The study included a group of 47 patients with chronic schizophrenia. Patients were assessed by means of PANSS, CGI, and a battery of cognitive tests: WCST, TMT, and verbal fluency test. MRI and MRS procedures were performed. Regions of interest were located in the left frontal lobe, temporal lobe and thalamus. Metabolite (NAA, choline, myoinositol and Glx complex) ratios to creatine were calculated. We observed a significant negative correlation between myoinositol level in the frontal lobe and WSCT test performance. These data were confirmed by further analysis, which showed a significant correlation between WCST outcome, negative symptoms score, education level and myoinositol ratio in the frontal lobe. When analyzing negative symptoms as independent variables, the analysis of regression revealed a significant relationship between negative symptoms score and verbal fluency score, together with choline level in the thalamus. The above data seem to confirm a significant role of the thalamus--a "transmission station" involved in connections with the prefrontal cortex--for psychopathology development (especially negative) in schizophrenia. Moreover, our results suggest that a neurodegenerative process may be involved in schizophrenia pathogenesis.
    Medical science monitor: international medical journal of experimental and clinical research 06/2012; 18(6):CR390-8. DOI:10.12659/MSM.882909 · 1.43 Impact Factor
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    • "Specifically, no effect of antipsychotic treatment was found on the increases in glutamate and glutamine in the anterior cingulate cortex of first episode patients for up to 30 months of treatment [120] or the increases in the glutamate / glutamine ratio in the anterior cingulate cortex for up to 12 months of treatment [132]. Similarly, no effects of risperidone on Glx levels in the frontal and temporal lobe or thalamus [148], or caudate nucleus [131] were detected. In contrast, one study suggests that antipsychotic treatment was able to restore thalamic glutamate concentrations to control levels [120]. "
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    ABSTRACT: Over the last 50 years, evidence for central involvement of glutamatergic neurotransmission in the pathophysiology of schizophrenia has accumulated. Recent advances in neuroimaging technology now allow several components of glutamatergic neurotransmission to be assessed in the living human brain. Positron emission tomography (PET) or single photon emission tomography (SPET) in combination with select radiotracers allows visualization of glutamatergic receptors in vivo, and magnetic resonance (MR) - based techniques allow mapping of the effects of glutamatergic agents on regional brain activation, and the measurement of regional glutamate concentrations. These imaging studies have provided evidence for regional glutamatergic abnormalities in psychosis, and are beginning to describe both the evolution of these abnormalities over the course of the illness and their response to therapeutic intervention. In parallel, advances in small animal imaging and the development of animal models have provided a platform to explore the neuropathological consequences of glutamatergic abnormality, and the potential antipsychotic efficacy of novel compounds. The molecular diversity of the glutamatergic system has driven the design of several compounds targeting aspects of glutamatergic transmission, and clinical trials have yielded encouraging results. Here, we review the contribution of imaging studies to date in understanding glutamatergic abnormalities in psychosis, and discuss the potential of new glutamatergic compounds for treatment of the disorder.
    Current pharmaceutical biotechnology 01/2012; 13(8):1500-12. DOI:10.2174/138920112800784961 · 2.51 Impact Factor
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