Diagnostic Performance of Ultrasonography for Identification of Small Bowel Obstruction; a Systematic Review and Meta-analysis.

Introduction: Small bowel obstruction (SBO) is known as a common cause of acute abdominal complaints in the emergency department (ED). The modality of choice for the diagnosis of SBO has not yet been established. This systematic review and meta-analysis aimed to investigate the accuracy of ultrasonography for the diagnosis of SBO. Methods: Systematic search was performed on five electronic databases including Medline, Scopus, Web of Sciences, Embase, and Cochrane Library, and the retrieval period was from the inception of each database to November 2023. The quality of the included studies were investigated using the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2). The pooled values of diagnostic characteristics for ultrasonography were estimated using meta-Disc and Stata statistical software. Results: Twenty-one studies with a total of 1977 patients were included in the meta-analysis. The pooled estimate for sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and area under the summary ROC curve of ultrasonography for diagnosing SBO were 0.93 (95% CI: 0.91-0.95), 0.8 (95% CI: 0.77-0.83), 5.69 (95% CI: 3.64-8.89), 0.1 (95% CI: 0.07-0.16), 83.51 (95% CI: 18.12-182.91) and 0.96, respectively. Conclusion: The findings of this meta-analysis showed that the utilization of ultrasonography holds promise as a diagnostic imaging for SBO with high accuracy. However, additional worldwide studies are essential to get more evidence on the value of ultrasonography for the diagnosis of SBO.

Diagnostic Performance of Artificial Intelligence in Detection of Primary Malignant Bone Tumors: a Meta-Analysis.

We aim to conduct a meta-analysis on studies that evaluated the diagnostic performance of artificial intelligence (AI) algorithms in the detection of primary bone tumors, distinguishing them from other bone lesions, and comparing them with clinician assessment. A systematic search was conducted using a combination of keywords related to bone tumors and AI. After extracting contingency tables from all included studies, we performed a meta-analysis using random-effects model to determine the pooled sensitivity and specificity, accompanied by their respective 95% confidence intervals (CI). Quality assessment was evaluated using a modified version of Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis (TRIPOD) and Prediction Model Study Risk of Bias Assessment Tool (PROBAST). The pooled sensitivities for AI algorithms and clinicians on internal validation test sets for detecting bone neoplasms were 84% (95% CI: 79.88) and 76% (95% CI: 64.85), and pooled specificities were 86% (95% CI: 81.90) and 64% (95% CI: 55.72), respectively. At external validation, the pooled sensitivity and specificity for AI algorithms were 84% (95% CI: 75.90) and 91% (95% CI: 83.96), respectively. The same numbers for clinicians were 85% (95% CI: 73.92) and 94% (95% CI: 89.97), respectively. The sensitivity and specificity for clinicians with AI assistance were 95% (95% CI: 86.98) and 57% (95% CI: 48.66). Caution is needed when interpreting findings due to potential limitations. Further research is needed to bridge this gap in scientific understanding and promote effective implementation for medical practice advancement.

Multiscale Modeling of Magnetoelectric Nanoparticles for the Analysis of Spatially Selective Neural Stimulation.

The growing field of nanoscale neural stimulators offers a potential alternative to larger scale electrodes for brain stimulation. Nanoelectrodes made of magnetoelectric nanoparticles (MENPs) can provide an alternative to invasive electrodes for brain stimulation via magnetic-to-electric signal transduction. However, the magnetoelectric effect is a complex phenomenon and challenging to probe experimentally. Consequently, quantifying the stimulation voltage provided by MENPs is difficult, hindering precise regulation and control of neural stimulation and limiting their practical implementation as wireless nanoelectrodes. The work herein develops an approach to determine the stimulation voltage for MENPs in a finite element analysis (FEA) model. This model is informed by atomistic material properties from ab initio Density Functional Theory (DFT) calculations and supplemented by experimentally obtainable nanoscale parameters. This process overcomes the need for experimentally inaccessible characteristics for magnetoelectricity, and offers insights into the effect of the more manageable variables, such as the driving magnetic field. The model's voltage is compared to in vivo experimental data to assess its validity. With this, a predictable and controllable stimulation is simulated by MENPs, computationally substantiating their spatial selectivity. This work proposes a generalizable and accessible method for evaluating the stimulation capability of magnetoelectric nanostructures, facilitating their realization as wireless neural stimulators in the future.

Artificial intelligence in osteoarthritis detection: A systematic review and meta-analysis.

OBJECTIVES: As an increasing number of studies apply artificial intelligence (AI) algorithms in osteoarthritis (OA) detection, we performed a systematic review and meta-analysis to pool the data on diagnostic performance metrics of AI, and to compare them with clinicians' performance. MATERIALS AND METHODS: A search in PubMed and Scopus was performed to find studies published up to April 2022 that evaluated and/or validated an AI algorithm for the detection or classification of OA. We performed a meta-analysis to pool the data on the metrics of diagnostic performance. Subgroup analysis based on the involved joint and meta-regression based on multiple parameters were performed to find potential sources of heterogeneity. The risk of bias was assessed using Prediction Model Study Risk of Bias Assessment Tool reporting guidelines. RESULTS: Of the 61 studies included, 27 studies with 91 contingency tables provided sufficient data to enter the meta-analysis. The pooled sensitivities for AI algorithms and clinicians on internal validation test sets were 88% (95% confidence interval [CI]: 86,91) and 80% (95% CI: 68,88) and pooled specificities were 81% (95% CI: 75,85) and 79% (95% CI: 80,85), respectively. At external validation, the pooled sensitivity and specificity for AI algorithms were 94% (95% CI: 90,97) and 91% (95% CI: 77,97), respectively. CONCLUSION: Although the results of this meta-analysis should be interpreted with caution due to the potential pitfalls in the included studies, the promising role of AI as a diagnostic adjunct to radiologists is indisputable.

Effect of Deep Brain Stimulation in The Ventral Tegmental Area on Neuronal Activity in Local and Remote Brain Regions in Kindled Mice.

OBJECTIVE: The mechanisms behind seizure suppression by deep brain stimulation (DBS) are not fully revealed, and the most optimal stimulus regimens and anatomical targets are yet to be determined. We investigated the modulatory effect of low-frequency DBS (L-DBS) in the ventral tegmental area (VTA) on neuronal activity in downstream and upstream brain areas in chemically kindled mice by assessing c-Fos immunoreactivity. MATERIALS AND METHODS: In this experimental study, 4-6 weeks old BL/6 male mice underwent stereotaxic implantation of a unilateral stimulating electrode in the VTA followed by pentylenetetrazole (PTZ) administration every other day until they showed stage 4 or 5 seizures following 3 consecutive PTZ injections. Animals were divided into control, sham-implanted, kindled, kindled-implanted, L-DBS, and kindled+L-DBS groups. In the L-DBS and kindled+L-DBS groups, four trains of L-DBS were delivered 5 min after the last PTZ injection. 48 hours after the last L-DBS, mice were transcardially perfused, and the brain was processed to evaluate c-Fos expression by immunohistochemistry. RESULTS: L-DBS in the VTA significantly decreased the c-Fos expressing cell numbers in several brain areas including the hippocampus, entorhinal cortex, VTA, substantia nigra pars compacta, and dorsal raphe nucleus but not in the amygdala and CA3 area of the ventral hippocampus compared to the sham group. CONCLUSION: These data suggest that the possible anticonvulsant mechanism of DBS in VTA can be through restoring the seizure-induced cellular hyperactivity to normal.

Brain-based Sex Differences in Depression: A Systematic Review of Neuroimaging Studies.

Major depressive disorder (MDD) is a common psychiatric illness with a wide range of symptoms such as mood decline, loss of interest, and feelings of guilt and worthlessness. Women develop depression more often than men, and the diagnostic criteria for depression mainly rely on female patients' symptoms. By contrast, male depression usually manifests as anger attacks, aggression, substance use, and risk-taking behaviors. Various studies have focused on the neuroimaging findings in psychiatric disorders for a better understanding of their underlying mechanisms. With this review, we aimed to summarize the existing literature on the neuroimaging findings in depression, separated by male and female subjects. A search was conducted on PubMed and Scopus for magnetic resonance imaging (MRI), functional MRI (fMRI), and diffusion tensor imaging (DTI) studies of depression. After screening the search results, 15 MRI, 12 fMRI, and 4 DTI studies were included. Sex differences were mainly reflected in the following regions: 1) total brain, hippocampus, amygdala, habenula, anterior cingulate cortex, and corpus callosum volumes, 2) frontal and temporal gyri functions, along with functions of the caudate nucleus and prefrontal cortex, and 3) frontal fasciculi and frontal projections of corpus callosum microstructural alterations. Our review faces limitations such as small sample sizes and heterogeneity in populations and modalities. But in conclusion, it reflects the possible roles of sex-based hormonal and social factors in the depression pathophysiology.

Optical coherence tomography angiography measurements in Parkinson's disease: A systematic review and meta-analysis.

Optical coherence tomography angiography (OCT-A) is an ocular imaging technology that has emerged as a non-invasive tool to evaluate retinal microvascular changes in neurodegenerative diseases including Parkinson's disease (PD) and Alzheimer's disease. While several studies have reported on the presence of pathologic retinal microvascular alterations in PD, the utility of OCT-A as a biomarker for PD evaluation is still unclear. A systematic review and meta-analysis were performed to explore the current evidence for the role of OCT-A in PD published up until June 2022. PubMed, Scopus, and Web of Science databases were used to systematically identify relevant papers and a meta-analysis was conducted using Stata16 software according to the level of heterogeneity applying a random- or fixed-effect model. Thirteen studies of 925 eyes in the PD group and 1501 eyes in the control group assessing OCT-A findings in PD patients were included. The meta-analyses revealed that the foveal region of PD patients had a significantly lower vessel density in the superficial capillary plexus (SCP) compared to healthy controls but that there were no significant differences in the foveal avascular zone, the SCP in whole, parafoveal, and perifoveal regions, and deep capillary plexus. OCT-A metrics may act as a potential biomarker for a more accurate and early PD diagnosis. Still, the OCT-A algorithms and interchangeability between OCT-A devices require further standardization to draw clinical conclusions regarding their utility.

White matter microstructural changes in internet addiction disorder: A systematic review of diffusion tensor imaging studies.

Diffusion tensor imaging (DTI) is a kind of magnetic resonance imaging (MRI) modality that helps designate tracts with brain microstructural changes. Internet gaming disorder (IGD) is an internet addiction that can cause many social and personality problems, such as problems in social communication, anxiety, and depression. There are several pieces of evidence showing the impact of this condition on brain regions, and many studies have investigated DTI measurements in these individuals. Therefore, we decided to systematically review the studies that have reported DTI parameters in IGD individuals. We searched the PubMed and Scopus databases to find relevant articles. Two reviewers separately screened the studies, and finally, 14 articles, including diffusion and network studies, were found eligible for our systematic review. Most of the studies reported findings on FA, showing an increase in the thalamus, anterior thalamic radiation, corticospinal tract, and inferior longitudinal fasciculus (ILF), while other regions mentioned in the studies demonstrated inconsistent findings. Moreover, in network studies, IGD individuals showed a decrease in nodal and global efficiencies. In conclusion, our study illuminates the neuropsychological basis of this condition and suggests that internet gaming can correlate with microstructural abnormalities in the central nervous system. Some correlate with the characteristics of online gaming, the addiction state, and the illness's duration.

Wireless stimulation of the subthalamic nucleus with nanoparticles modulates key monoaminergic systems similar to contemporary deep brain stimulation.

BACKGROUND: Deep brain stimulation (DBS) is commonly used to alleviate motor symptoms in several movement disorders. However, the procedure is invasive, and the technology has remained largely stagnant since its inception decades ago. Recently, we have shown that wireless nanoelectrodes may offer an alternative approach to conventional DBS. However, this method is still in its infancy, and more research is required to characterize its potential before it can be considered as an alternative to conventional DBS. OBJECTIVES: Herein, we aimed to investigate the effect of stimulation via magnetoelectric nanoelectrodes on primary neurotransmitter systems that have implications for DBS in movement disorders. METHODS: Mice were injected with either magnetoelectric nanoparticles (MENPs) or magnetostrictive nanoparticles (MSNPs, as a control) in the subthalamic nucleus (STN). Mice then underwent magnetic stimulation, and their motor behavior was assessed in the open field test. In addition, magnetic stimulation was applied before sacrifice and post-mortem brains were processed for immunohistochemistry (IHC) to assess the co-expression of c-Fos with either tyrosine hydroxylase (TH), tryptophan hydroxylase-2 (TPH2) or choline acetyltransferase (ChAT). RESULTS: Stimulated animals covered longer distances in the open field test when compared to controls. Moreover, we found a significant increase in c-Fos expression in the motor cortex (MC) and paraventricular region of the thalamus (PV-thalamus) after magnetoelectric stimulation. Stimulated animals showed fewer TPH2/c-Fos double-labeled cells in the dorsal raphe nucleus (DRN), as well as TH/c-Fos double-labeled cells in the ventral tegmental area (VTA), but not in the substantia nigra pars compacta (SNc). There was no significant difference in the number of ChAT/ c-Fos double-labeled cells in the pedunculopontine nucleus (PPN). CONCLUSIONS: Magnetoelectric DBS in mice enables selective modulation of deep brain areas and animal behavior. The measured behavioral responses are associated with changes in relevant neurotransmitter systems. These changes are somewhat similar to those observed in conventional DBS, suggesting that magnetoelectric DBS might be a suitable alternative.

The role of neurotransmitter systems in mediating deep brain stimulation effects in Parkinson's disease.

Deep brain stimulation (DBS) is among the most successful paradigms in both translational and reverse translational neuroscience. DBS has developed into a standard treatment for movement disorders such as Parkinson's disease (PD) in recent decades, however, specific mechanisms behind DBS's efficacy and side effects remain unrevealed. Several hypotheses have been proposed, including neuronal firing rate and pattern theories that emphasize the impact of DBS on local circuitry but detail distant electrophysiological readouts to a lesser extent. Furthermore, ample preclinical and clinical evidence indicates that DBS influences neurotransmitter dynamics in PD, particularly the effects of subthalamic nucleus (STN) DBS on striatal dopaminergic and glutamatergic systems; pallidum DBS on striatal dopaminergic and GABAergic systems; pedunculopontine nucleus DBS on cholinergic systems; and STN-DBS on locus coeruleus (LC) noradrenergic system. DBS has additionally been associated with mood-related side effects within brainstem serotoninergic systems in response to STN-DBS. Still, addressing the mechanisms of DBS on neurotransmitters' dynamics is commonly overlooked due to its practical difficulties in monitoring real-time changes in remote areas. Given that electrical stimulation alters neurotransmitter release in local and remote regions, it eventually exhibits changes in specific neuronal functions. Consequently, such changes lead to further modulation, synthesis, and release of neurotransmitters. This narrative review discusses the main neurotransmitter dynamics in PD and their role in mediating DBS effects from preclinical and clinical data.

High-frequency stimulation of the subthalamic nucleus induces a sustained inhibition of serotonergic system via loss of cell phenotype.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has become a standard treatment for Parkinson's disease (PD). However, in a considerable number of patients debilitating psychiatric side-effects occur. Recent research has revealed that external stimuli can alter the neurotransmitters' homeostasis in neurons, which is known as "neurotransmitter respecification". Herein, we addressed if neurotransmitter respecification could be a mechanism by which DBS suppresses the serotonergic function in the dorsal raphe nucleus (DRN) leading to mood changes. We infused transgenic 5-HT-Cre (ePET-Cre) mice with AAV viruses to achieve targeted expression of eYFP and the genetically encoded calcium indicator GCaMP6s in the DRN prior to methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Mice received bilateral DBS electrodes in the STN and an optic fiber in the DRN for calcium photometry. MPTP-treated mice demonstrated behavioral and histological PD phenotype, whereas all STN-DBS animals exhibited an increased immobility time in the forced swim test, reduced calcium activity, and loss of tryptophan hydroxylase-2 expression in the DRN. Given the prominent role of calcium transients in mediating neurotransmitter respecification, these results suggest a loss of serotonergic phenotype in the DRN following STN-DBS. These findings indicate that loss of serotonergic cell phenotype may underlie the unwanted depressive symptoms following STN-DBS.

Post-Mortem Analysis of Neuropathological Changes in Human Tinnitus.

Tinnitus is the phantom perception of a sound, often accompanied by increased anxiety and depressive symptoms. Degenerative or inflammatory processes, as well as changes in monoaminergic systems, have been suggested as potential underlying mechanisms. Herein, we conducted the first post-mortem histopathological assessment to reveal detailed structural changes in tinnitus patients' auditory and non-auditory brain regions. Tissue blocks containing the medial geniculate body (MGB), thalamic reticular nucleus (TRN), central part of the inferior colliculus (CIC), and dorsal and obscurus raphe nuclei (DRN and ROb) were obtained from tinnitus patients and matched controls. Cell density and size were assessed in Nissl-stained sections. Astrocytes and microglia were assessed using immunohistochemistry. The DRN was stained using antibodies raised against phenylalanine hydroxylase-8 (PH8) and tyrosine-hydroxylase (TH) to visualize serotonergic and dopaminergic cells, respectively. Cell density in the MGB and CIC of tinnitus patients was reduced, accompanied by a reduction in the number of astrocytes in the CIC only. Quantification of cell surface size did not reveal any significant difference in any of the investigated brain regions between groups. The number of PH8-positive cells was reduced in the DRN and ROb of tinnitus patients compared to controls, while the number of TH-positive cells remained unchanged in the DRN. These findings suggest that both neurodegenerative and inflammatory processes in the MGB and CIC underlie the neuropathology of tinnitus. Moreover, the reduced number of serotonergic cell bodies in tinnitus cases points toward a potential role of the raphe serotonergic system in tinnitus.

The Effect of Noise Trauma and Deep Brain Stimulation of the Medial Geniculate Body on Tissue Activity in the Auditory Pathway.

Tinnitus is defined as the phantom perception of sound. To date, there is no curative treatment, and contemporary treatments have failed to show beneficial outcomes. Deep brain stimulation has been suggested as a potential therapy for refractory tinnitus. However, the optimal target and stimulation regimens remain to be defined. Herein, we investigated metabolic and neuronal activity changes using cytochrome C oxidase histochemistry and c-Fos immunohistochemistry in a noise trauma-induced rat model of tinnitus. We also assessed changes in neuronal activity following medial geniculate body (MGB) high-frequency stimulation (HFS). Metabolic activity was reduced in the primary auditory cortex, MGB and CA1 region of the hippocampus in noise-exposed rats. Additionally, c-Fos expression was increased in the primary auditory cortex of those animals. Furthermore, MGB-HFS enhanced c-Fos expression in the thalamic reticular nucleus. We concluded that noise trauma alters tissue activity in multiple brain areas including the auditory and limbic regions. MGB-HFS resulted in higher neuronal activity in the thalamic reticular nucleus. Given the prominent role of the auditory thalamus in tinnitus, these data provide more rationales towards targeting the MGB with HFS as a symptom management tool in tinnitus.

Nigral neuropathology of Parkinson's motor subtypes coincide with circuitopathies: a scoping review.

The neuropathological substrates of Parkinson's disease (PD) patients with motor subtypes tremor-dominance (TD), non-tremor dominance (nTD), postural instability and gait difficulty (PIGD), and akinetic-rigid (AR) are not completely differentiated. While extensive pathological research has been conducted on neuronal tissue of PD patients, data have not been discussed in the context of mechanistic circuitry theories differentiating motor subtypes. It is, therefore, expected that a more specific and tailored management of PD symptoms can be accomplished by understanding symptom-specific neuropathological mechanisms with the detail histology can provide. This scoping review gives an overview of the literature comparing TD and nTD PD motor subtypes by clarify observed pathology with underlying physiological circuitry theories. Studies using an array of pathological examination techniques have shown significant differences between TD and nTD PD subtypes. nTD PD patients show higher neuronal loss, gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in multiple subregions of the substantia nigra (SN) related to the overactivity of the indirect motor loop. TD patients show more severe cell loss specifically in medial SN subdivisions, and have damage in the retrorubral field A-8 that projects to the dorsolateral striatum and ventromedial thalamus in the direct motor loop. Pathological studies are consistent with neuroimaging data and support contemporary mechanistic circuitry theories of PD motor symptom genesis. Further multimodal neuroimaging and histological studies are required to validate and expand upon these findings.

Deep brain stimulation of the nucleus basalis of Meynert in an experimental rat model of dementia: Stimulation parameters and mechanisms.

BACKGROUND/OBJECTIVE: Deep brain stimulation (DBS) of the nucleus basalis of Meynert (NBM) has gained interest as a potential therapy for treatment-resistant dementia. However, optimal stimulation parameters and mechanisms of action are yet to be elucidated. METHODS: First, we assessed NBM DBS at different stimulation parameters in a scopolamine-induced rat model of dementia. Rats were tested in the object location task with the following conditions: (i) low and high frequency (20 Hz or 120 Hz), (ii) monophasic or biphasic pulse shape (iii) continuous or intermittent DBS (20s on, 40s off) and 100 µA amplitude. Thereafter, rats were stimulated with the most effective parameter followed by 5-bromo-2'-deoxyuridine (BrdU) administration and perfused 4 weeks later. We then evaluated the effects of NBM DBS on hippocampal neurogenesis, synaptic plasticity, and on cholinergic fibres in the perirhinal and cingulate cortex using immunohistochemistry. We also performed in-vivo microdialysis to assess circuit-wide effects of NBM DBS on hippocampal acetylcholine levels during on and off stimulation. RESULTS: Biphasic, low frequency and intermittent NBM DBS reversed the memory impairing effects of scopolamine when compared to sham rats. We found that acute stimulation promoted proliferation in the dentate gyrus, increased synaptic plasticity in the CA1 and CA3 subregion of the hippocampus, and increased length of cholinergic fibres in the cingulate gyrus. There was no difference regarding hippocampal acetylcholine levels between the groups. CONCLUSION: These findings suggest that the potential mechanism of action of the induced memory enhancement through NBM DBS might be due to selective neuroplastic and neurochemical changes.

The role of the medial geniculate body of the thalamus in the pathophysiology of tinnitus and implications for treatment.

Tinnitus is an auditory sensation in the absence of actual external stimulation. Different clinical interventions are used in tinnitus treatment, but only few patients respond to available options. The lack of successful tinnitus treatment is partly due to the limited knowledge about the mechanisms underlying tinnitus. Recently, the auditory part of the thalamus has gained attention as a central structure in the neuropathophysiology of tinnitus. Increased thalamic spontaneous firing rate, bursting activity and oscillations, alongside an increase of GABAergic tonic inhibition have been shown in the auditory thalamus in animal models of tinnitus. In addition, clinical neuroimaging studies have shown structural and functional thalamic changes with tinnitus. This review provides a systematic overview and discussion of these observations that support a central role of the auditory thalamus in tinnitus. Based on this approach, a neuromodulative treatment option for tinnitus is proposed.