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Diffusion tensor imaging (DTI) studies in patients with schizophrenia have shown abnormalities in the microstructure of white matter tracts. Specifically, reduced fractional anisotropy (FA) has been described across multiple white matter tracts, in studies that have mainly included patients treated with antipsychotic medications.To compare FA in antipsychotic-naïve patients experiencing a first episode of psychosis (FEP) to FA in healthy controls to demonstrate that the variance of FA can be grouped, in a coincidental manner, in four predetermined factors in accordance with a theoretical partition of the white matter tracts, using a principal components analysis (PCA).Thirty-five antipsychotic-naïve FEP patients and 35 age- and gender-matched healthy controls underwent DTI at 3T. Analysis was performed using a tract-based spatial statistics (TBSS) method and exploratory PCA.DTI analysis showed extensive FA reduction in white matter tracts in FEP patients compared with the control group. The PCA grouped the white matter tracts into four factors explaining 66% of the total variance. Comparison of the FA values within each factor highlighted the differences between FEP patients and controls.Our study confirms extensive white matter tracts anomalies in patients with schizophrenia, more specifically, in drug-naïve FEP patients. The results also indicate that a small number of white matter tracts share common FA anomalies that relate to deficit symptoms in FEP patients. Our study adds to a growing body of literature emphasizing the need for treatments targeting white matter function and structure in FEP patients.

Huntington's disease is an hereditary autosomic-dominant neurodegenerative disorder, characterized by motor, cognitive and psychiatric symptoms.To quantify differences in N-acetylaspartate, creatine and choline in caudate nucleus, putamen and occipital cortex of patients with Huntington's disease, symptomatics and asymptomatics.Hydrogen magnetic resonance spectroscopy was performed with a 3 T scanner in 10 Huntington's disease gene-tested subjects, included in three groups: negative (control), positive symptomatics and positive asymptomatics. Data was quantified with LCModel and analyzed with ANOVA and Fisher tests.Symptomatic patients showed decreased creatine and N-acetylaspartate in the three regions, and decreased choline only in putamen (p0.05). Choline difference was found between symptomatics and asymptomatics in the caudate nucleus (p0.05).Results may reflect neuronal dysfunction and suggest that creatine and choline may serve as markers for Huntington's disease progression.

Importance Increased glutamate levels in the right associative striatum have been described in patients during a first episode of psychosis. Whether this increase would persist after effective antipsychotic treatment is unknown. Objectives To compare the glutamate levels in antipsychotic-naive patients with first-episode psychosis in the right associative striatum and right cerebellar cortex using proton magnetic resonance spectroscopy before and 4 weeks after antipsychotic treatment and to compare these results with normative data from sex-matched healthy control subjects. Design, Setting, and Participants Before-after trial in an inpatient psychiatric research unit among 24 antipsychotic-naive patients with first-episode psychosis and 18 healthy controls matched for age, sex, handedness, and cigarette smoking. Interventions Participants underwent 2 proton magnetic resonance spectroscopy studies: patients were imaged at baseline and after 4 weeks of antipsychotic treatment, while controls were imaged at baseline and at 4 weeks after the baseline measurement. Patients were treated with oral risperidone (open label) for 4 weeks with dosages that were titrated on the basis of clinical judgment. Main Outcomes and Measures Glutamate levels were estimated using LCModel (version 6.2-1T) and were corrected for the cerebrospinal fluid proportion within the voxel. Results Patients with first-episode psychosis had higher levels of glutamate in the associative striatum and the cerebellum during the antipsychotic-naive condition compared with controls. After clinically effective antipsychotic treatment, glutamate levels significantly decreased in the associative striatum, with no significant change in the cerebellum. No differences in glutamate levels were observed between groups at 4 weeks. Conclusions and Relevance Increased glutamate levels observed at baseline in patients with first-episode psychosis normalized after 4 weeks of clinically effective antipsychotic treatment. These results provide support for the hypothesis that improvement in clinical symptoms might be related to a decrease in glutamate levels.

Introduccion. La enfermedad de Huntington es un trastorno neurodegenerativo hereditario autosomico dominante, caracterizado por sintomas motores, cognitivos y psiquiatricos. Objetivo. Determinar si existen diferencias en las concentraciones de N-acetilaspartato, creatina y compuestos que contienen colina (glucerilfosforilcolina y fosfocolina) en el nucleo caudado, el putamen y la corteza occipital de pacientes con enfermedad de Huntington, sintomaticos y asintomaticos. Sujetos y metodos. Se realizaron estudios de espectroscopia de hidrogeno por resonancia magnetica en un equipo de 3 T a 10 individuos con prueba genetica para enfermedad de Huntington, incluidos en tres grupos: negativos (control), positivos sintomaticos y positivos asintomaticos. Los estudios se cuantificaron con LCModel y se analizaron mediante analisis de varianza y prueba de Fisher. Resultados. Los pacientes sintomaticos mostraron disminucion de creatina y N-acetilaspartato en las regiones estudiadas, y disminucion de colina en el putamen (p < 0,05). En el nucleo caudado se encontro diferencia de colina entre sintomaticos y asintomaticos (p < 0,05). Conclusiones. Los resultados reflejan disfuncion en el metabolismo neuronal y sugieren que la creatina y la colina, al ser marcadores de membrana, pueden comportarse en forma indirecta como marcadores de la evolucion en la enfermedad de Huntington.