OBJECTIVE: Parkinson\'s disease (PD) involves pathological alterations that include cortical impairments at levels of region and network. However, its microstructural abnormalities remain to be further elucidated via an appropriate diffusion neuroimaging approach. This study aimed to comprehensively demonstrate the microstructural patterns of PD as mapped by diffusion kurtosis imaging (DKI).
METHODS: The microstructure of grey matter in both the PD group and the matched healthy control group was quantified by a DKI metric (mean kurtosis). The intergroup difference and classification performance of global microstructural complexity were analyzed in a voxelwise manner and via a machine learning approach, respectively. The patterns of information flows were explored in terms of structural connectivity, network covariance and modular connectivity.
RESULTS: Patients with PD exhibited global microstructural impairments that served as an efficient diagnostic indicator. Disrupted structural connections between the striatum and cortices as well as between the thalamus and cortices were widely distributed in the PD group. Aberrant covariance of the striatocortical circuitry and thalamocortical circuitry was observed in patients with PD, who also showed disrupted modular connectivity within the striatum and thalamus as well as across structures of the cortex, striatum and thalamus.
CONCLUSIONS: These findings verified the potential clinical application of DKI for the exploration of microstructural patterns in PD, contributing complementary imaging features that offer a deeper insight into the neurodegenerative process.

Working memory (WM) is considered as the scratchpad for reading, writing, and processing information necessary to perform cognitive tasks. The Basal Ganglia (BG) and Prefrontal Cortex are two important parts of the brain that are involved in WM functions, and both structures receive projections from dopaminergic nuclei. In this modelling study, we specifically focus on modelling the WM functions of the BG, the WM deficits in Parkinson\'s disease (PD) conditions, and the impact of dopamine deficiency on different kinds of WM functions. Though there are many experimental and modelling studies of WM properties, there is a paucity of models of the BG that provide insights into the contributions of the BG in WM functions. The proposed model of BG uses bistable flip-flop neurons to model striatal up-down neurons, a network of nonlinear oscillators to model the oscillations of the Indirect Pathway of BG and race-model for action selection. Five different WM tasks are used to demonstrate the generalisation ability of the proposed model. Experimental data from the four tasks are compared with model performance in both control and PD conditions. The model is extended to predict the response time of subjects and in the PD version of the model, the effect of dopaminergic medication on WM performance is also simulated. The proposed model of BG is a unified model that can explain the WM functions of the BG over a wide variety of tasks in both normal and PD conditions, and can be used to understand why specific WM functions are impaired whereas others remain intact in PD.
UNASSIGNED: The online version contains supplementary material available at 10.1007/s11571-023-10056-y.

BACKGROUND: The blink reflex excitability, assessed through paired electrical stimuli responses, has been modulated using traditional non-invasive neurostimulation techniques. Recently, transcranial Alternating Current Stimulation (tACS) emerged as a tool to modulate brain oscillations implicated in various motor, perceptual, and cognitive functions. This study aims to investigate the influence of 20-Hz and 10-Hz tACS sessions on the primary motor cortex and their impact on blink reflex excitability.
METHODS: Fifteen healthy volunteers underwent 10-min tACS sessions (intensity 1 mA) with active/reference electrodes placed over C4/Pz, delivering 20-Hz, 10-Hz, and sham stimulation. The blink reflex recovery cycle (BRrc) was assessed using the R2 amplitude ratio at various interstimulus intervals (ISIs) before (T0), immediately after (T1), and 30 min post-tACS (T2).
RESULTS: Both 10-Hz and 20-Hz tACS sessions significantly increased R2 ratio at T1 (10-Hz: p = 0.02; 20-Hz: p < 0.001) and T2 (10-Hz: p = 0.01; 20-Hz: p < 0.001) compared to baseline (T0). Notably, 20-Hz tACS induced a significantly greater increase in blink reflex excitability compared to sham at both T1 (p = 0.04) and T2 (p < 0.001).
CONCLUSIONS: This study demonstrates the modulatory effect of tACS on trigemino-facial reflex circuits, with a lasting impact on BRrc. Beta-band frequency tACS exhibited a more pronounced effect than alpha-band frequency, highlighting the influential role of beta-band oscillations in the motor cortex on blink reflex excitability modulation.

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UNASSIGNED: Multiple sclerosis (MS) is an inflammatory demyelinating and neurodegenerative disorder of the central nervous system, which is associated with brain atrophy and volume changes in some brain structures. This study aimed to compare the volume of the basal ganglia, thalamus, cerebellum, and brainstem in patients with relapsing-remitting MS with that of the control group using magnetic resonance imaging (MRI).
UNASSIGNED: In this cross-sectional study, MRI brain scans were obtained from 25 patients with relapsing-remitting MS and 25 healthy control subjects. Volumetric analyses were performed using Brain Suite software.
UNASSIGNED: The mean age of the MS and the control groups was 33.96±8.75 and 40.40±8.72, respectively. No statistically significant difference was found in gender (P=0.747). The bilateral putamen and caudate nuclei volumes were significantly higher in the case group than in the control group (P<0.001). Moreover, lower the volume of the brainstem, cerebellum, bilateral thalamus, and globus pallidus were identified in the MS patients compared to the control group (P<0.001). There was an inverse correlation between the disease and treatment duration with the thalamus and cerebellum volume in MS patients (P=0.001). Treatment duration also had an inverse correlation with brainstem volume (P=0.047).
UNASSIGNED: The volume of some structures of the brain, including globus pallidus, thalamus, cerebellum, and brainstem is lower in MS and can be one of the markers of disease progression and disability among MS patients.
UNASSIGNED: Due to the degenerative process in multiple sclerosis, some cerebral structures may face volume change.The present study demonstrated that the volume of globus pallidus, thalamus, cerebellum, and brainstem is lower in MS patients compared to the controls.
UNASSIGNED: Multiple sclerosis (MS) is defined as an inflammatory disease involving the white matter of the brain, but experience has shown that many non-white matter structures also change in MS. In this study, we aimed to examine some parts of the brain, such as the thalamus, basal ganglia, brainstem, and cerebellum, for volume changes. The results showed that all these structures can have a smaller volume in MS patients than in healthy people. Especially in the case of the thalamus and cerebellum, this difference increases with increasing the disease duration. Changes in the size of these structures can be the result of degeneration of the neurons in these areas. These changes can cause significant disability in patients; however, there may not be significant changes in the number of plaques in patients. Attention to these changes can be essential in interpreting patients\' clinical changes, including motor and cognitive disabilities.

The subthalamic nucleus (STN) is traditionally thought to restrict movement. Lesion or prolonged STN inhibition increases movement vigor and propensity, while optogenetic excitation has opposing effects. However, STN neurons often exhibit movement-related increases in firing. To address this paradox, STN activity was recorded and manipulated in head-fixed mice at rest and during self-initiated and self-paced treadmill locomotion. We found that (1) most STN neurons (type 1) exhibit locomotion-dependent increases in activity, with half firing preferentially during the propulsive phase of the contralateral locomotor cycle; (2) a minority of STN neurons exhibit dips in activity or are uncorrelated with movement; (3) brief optogenetic inhibition of the lateral STN (where type 1 neurons are concentrated) slows and prematurely terminates locomotion; and (4) in Q175 Huntington\'s disease mice, abnormally brief, low-velocity locomotion is associated with type 1 hypoactivity. Together, these data argue that movement-related increases in STN activity contribute to optimal locomotor performance.

The cerebral cortex has long been thought to be involved in the pathophysiology of motor symptoms of Parkinson\'s disease. The impaired cortical function is believed to be a direct and immediate effect of pathologically patterned basal ganglia output, mediated to the cerebral cortex by way of the ventral motor thalamus. However, recent studies in humans with Parkinson\'s disease and in animal models of the disease have provided strong evidence suggesting that the involvement of the cerebral cortex is much broader than merely serving as a passive conduit for subcortical disturbances. In the present review, we discuss Parkinson\'s disease-related changes in frontal cortical motor regions, focusing on neuropathology, plasticity, changes in neurotransmission, and altered network interactions. We will also examine recent studies exploring the cortical circuits as potential targets for neuromodulation to treat Parkinson\'s disease.

Background/Objectives: Magnetic Resonance Imaging (MRI) is essential in diagnosing neurological conditions, offering detailed insights into brain pathology. Uremic encephalopathy (UE) is a severe neurological disorder resulting from renal failure, characterized by cognitive impairments and brain abnormalities due to the accumulation of uremic toxins (UTs). Despite extensive research on UTs, there is a significant gap in the detailed characterization of MRI findings in UE patients. This study aims to bridge this gap by conducting a comprehensive literature review of cerebral MRI findings in UE. We hypothesize that specific MRI patterns correlate with the severity and clinical manifestations of UE, thereby enhancing diagnostic accuracy and improving patient outcomes. Methods: A literature review was performed using PubMed, Cochrane Library, and Google Scholar. The search terms included \"uremic encephalopathy MRI\", \"uremia and kidney failure MRI\", and \"toxic and metabolic or acquired encephalopathies MRI\". The inclusion criteria were original articles on UE and MRI findings published in English. Results: Common MRI sequences include T1-weighted, T2-weighted, FLAIR, and DWI. Frequent MRI findings in UE are cytotoxic and vasogenic brain edema in regions such as the basal ganglia and periventricular white matter. Patterns like the \"lentiform fork sign\" and basal ganglia involvement are key indicators of UE. Conclusions: MRI plays a crucial role in diagnosing UE by identifying characteristic brain edema and specific patterns. A comprehensive diagnostic approach, incorporating clinical, laboratory, and imaging data, is essential for accurate diagnosis and management. The study calls for larger well-designed cohorts with long-term follow-up to improve the understanding and treatment of UE.

Aim: Neurological manifestations are common in patients with chronic liver diseases. This study aimed to depict the association between liver cirrhosis and Parkinson\'s disease (PD) and propose a clinically relevant diagnostic scheme. Methods: We examined patients\' medical records with PD and chronic liver impairment secondary to cirrhosis or liver metastases for temporal correlations between liver insult and Parkinsonian signs. Results: Thirty-five individuals with PD and chronic liver impairment were included due to either cirrhosis or liver metastases. In all 22 patients with PD and liver metastases, the diagnosis of PD preceded the diagnosis of cancer. Conversely, patients with cirrhosis were often diagnosed with liver impairment before diagnosing PD. Age at diagnosis did not account for this difference. Conclusions: This study reinforces the potential clinical association between cirrhosis and PD. We also provide a diagnostic scheme that may guide therapeutic interventions and prognostic assessments.