High doses of antipsychotics have been associated with loss in cortical and total gray matter in schizophrenia. However, previous imaging studies have not taken benzodiazepine use into account, in spite of evidence suggesting adverse effects such as cognitive impairment and increased mortality. In this Northern Finland Birth Cohort 1966 study, 69 controls and 38 individuals with schizophrenia underwent brain MRI at the ages of 34 and 43 years. At baseline, the average illness duration was over 10 years. Brain structures were delineated using an automated volumetry system, volBrain, and medication data on cumulative antipsychotic and benzodiazepine doses were collected using medical records and interviews. We used linear regression with intracranial volume and sex as covariates; illness severity was also taken into account. Though both medication doses associated to volumetric changes in subcortical structures, after adjusting for each other and the average PANSS total score, higher scan-interval antipsychotic dose associated only to volume increase in lateral ventricles and higher benzodiazepine dose associated with volume decrease in the caudate nucleus. To our knowledge, there are no previous studies reporting associations between benzodiazepine dose and brain structural changes. Further studies should focus on how these observations correspond to cognition and functioning.
We compared eleven OCT devices in their ability to quantify retinal layer thicknesses under different signal-strength conditions, using a commercially available phantom eye. We analyzed a medium-intensity 50 µm layer in an identical manner for all devices, using the provided log-scale images and a reconstructed linear-scale tissue reflectivity metric. Thickness measurements were highly comparable when the data were analyzed in an identical manner. With optimal signal strength, the thickness of the 50 µm layer was overestimated by a mean of 4.3 µm in the log-scale images and of 2.7 µm in the linear-scale images.
Glaucomatous damage can be quantified by measuring the thickness of different retinal layers. However, poor image quality may hamper the accuracy of the layer thickness measurement. We determined the effect of poor image quality (low signal-to-noise ratio) on the different layer thicknesses and compared different segmentation algorithms regarding their robustness against this degrading effect. For this purpose, we performed OCT measurements in the macular area of healthy subjects and degraded the image quality by employing neutral density filters. We also analysed OCT scans from glaucoma patients with different disease severity. The algorithms used were: The Canon HS-100’s built-in algorithm, DOCTRAP, IOWA, and FWHM, an approach we developed. We showed that the four algorithms used were all susceptible to noise at a varying degree, depending on the retinal layer assessed, and the results between different algorithms were not interchangeable. The algorithms also differed in their ability to differentiate between young healthy eyes and older glaucoma eyes and failed to accurately separate different glaucoma stages from each other.
The aim of this paper was to investigate differences in brain structure volumes between schizophrenia and affective psychoses, and whether cumulative lifetime antipsychotic or benzodiazepine doses relate to brain morphology in these groups. We conducted two systematic reviews on the topic and investigated 44 schizophrenia cases and 19 with affective psychoses from the Northern Finland Birth Cohort 1966. The association between lifetime antipsychotic and benzodiazepine dose and brain MRI scans at the age of 43 was investigated using linear regression. Intracranial volume, sex, illness severity, and antipsychotic/benzodiazepine doses were used as covariates. There were no differences between the groups in brain structure volumes. In schizophrenia, after adjusting for benzodiazepine dose and symptoms, a negative association between lifetime antipsychotic dose and the nucleus accumbens volume remained. In affective psychoses, higher lifetime benzodiazepine dose associated with larger volumes of total gray matter and hippocampal volume after controlling for antipsychotic use and symptoms. It seems that in addition to antipsychotics, the severity of symptoms and benzodiazepine dose are also associated with brain structure volumes. These results suggest, that benzodiazepine effects should also be investigated also independently and not only as a confounder.
Glaucoma is a chronic and progressive eye disease that leads to thinning of the retinal nerve fibre layer (RNLF) and the ganglion cell layer (GCL). Optical coherence tomography (OCT) allowed for a detailed assessment of these layers.
IntroductionThe effects of long-term antipsychotic medication use on structural brain changes in psychoses are still unknown. Severity and duration of illness are key confounders when evaluating antipsychotic effects on brain morphology.ObjectivesUnderstanding the role of antipsychotic medication on brain morphology in psychoses.AimsTo analyze whether cumulative lifetime or current antipsychotic medication dose relates to brain morphology in schizophrenia and other psychoses at age of 43 years.MethodsForty-four schizophrenia cases and 35 with other psychoses from the Northern Finland Birth Cohort 1966 were scanned on a 1.5T GE Signa scanner and brain structures were extracted using volBrain automated volumetry system (http://volbrain.upv.es). Data of antipsychotic medication were collected from medical records and interviews. We used linear regression model to analyze the effect of antipsychotic medication on brain volumes and used intracranial volume and onset age as covariates. We also performed additional analyses adding psychotic symptoms (PANSS Total score) as a covariate.ResultsHigher lifetime and current dose associated to left lateral ventricle increase (b = 0.33, P = 0.033; b = 0.307, P = 0.042, respectively) and right and left accumbens decrease (b = −0.405, P = 0.013, b = −0.404, P = 0.010; b = −0.302, P = 0.027, b = −0.282, P = 0.036, respectively) in schizophrenia but not in other psychoses. When PANSS was added to the model, the findings remained regarding right and left accumbens, but not regarding left lateral ventricle.ConclusionsIt seems that antipsychotic medication affects the brain in schizophrenia, but not in the heterogeneous group of other psychoses. In schizophrenia, brain changes associated to antipsychotic medication cannot be explained by illness duration or symptom severity.Disclosure of interestThe authors have not supplied their declaration of competing interest.
Results: Violent SCZ patients had increased cortical folding in the visual (lateral occipital) cortex bilaterally and left lateral orbitofrontal cortex compared to nonviolent SCZ patients. Compared to HC, violent SCZ folding patterns differed in the lateral orbitofrontal-, inferior temporal-, inferior parietal-, supramarginal-, postcentral-, lingual-, and pericalcarine cortex. Violent SCZ patients had reduced cortical thickness in the left precentral-, inferior parietal-, superior temporal-and the right fusiform cortex compared to nonviolent SCZ patients, and reduced thickness in the left fusiform-and right inferior parietal-, superior frontal-, and lingual cortex compared to HC. There were no group differences in cortical volume or area. Conclusion: Violent SCZ patients show regionally reduced cortical thickness and increased folding compared to nonviolent SCZ patients. Differences were found in cortical areas involved in visual and auditive processing, face and emotion recognition, and emotion and reward in decisionmaking. While the timing and origin of the cortical thickness reduction could reflect several genetic, disease-related or environmental factors, the cortical folding abnormalities suggests that aberrant neurodevelopment is of importance to violence in SCZ. Future studies are needed to explore the functional consequences of the observed differences. Background: High doses of antipsychotic medication have been associated with loss in cortical and total gray matter in schizophrenia, but the studies have not adjusted for benzodiazepine use. There are no modern imaging studies on the effects of benzodiazepine on brain structures in spite of evidence suggesting adverse effects such as cognitive impairment and increased mortality. Methods: In this study we examined the association between cumulative antipsychotic and benzodiazepine dose and brain volume change in schizophrenia cases with average illness duration over 10 years at baseline. Thirtyeight individuals with schizophrenia and 69 controls from the Northern Finland Birth Cohort 1966 went through brain MRI at the ages of 34 and 43 years (9-year follow-up). Brain structures were delineated from MRIs using an automated volumetry system, volBrain. Medication use data were collected using medical records and interviews. The data were analyzed with linear regression using intracranial volume and sex as covariates; illness severity was also taken into account. Results: Both antipsychotic and benzodiazepine dose during the scan interval associated statistically significantly to volumetric changes in subcortical structures. However, after adjusting for each other and the average PANSS total score, higher scan-interval antipsychotic dose associated only to volume increase in lateral ventricles (b = 0.502, P = .028) and higher benzodiazepine dose associated with volume decrease in the caudate nucleus (b = −0.422, P = .029). Conclusion: To our knowledge, this is the first study to report associations between benzodiazepine dose and brain structural changes in s...
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