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Background: The traditional diagnostic methods for early hepatic encephalopathy (HE) detection involve certain limitations, including subjectivity and low sensitivity. This study aimed to integrate synthetic magnetic resonance imaging (SyMRI) and quantitative susceptibility mapping (QSM) techniques to examine the changes in quantitative parameter values of patients with hepatitis B virus-related (HBV-related) decompensated cirrhosis, with the goal of providing imaging-based evidence for early neurological symptoms and disease monitoring in patients with cirrhosis.
Methods: Data from 41 patients with HBV-related decompensated cirrhosis and 40 healthy controls were prospectively collected. T1 values, T2 values, proton density (PD) values, and magnetic susceptibility values of the bilateral frontal white matter, parietal white matter, occipital white matter, caudate nuclei, putamen, globus pallidus, thalamus, substantia nigra, red nuclei, and dentate nuclei were measured. Analysis of covariance (ANCOVA) was used to compare these values between the two groups. P values obtained were then corrected via the false-discovery rate (FDR) method. Correlation analysis was used to determine the correlation between the brain quantitative parameter values of patients and their clinical indicators.
Results: In the SyMRI study, patients with cirrhosis had significantly lower T1 values in the right frontal white matter (RFWM) (P=0.030), left frontal white matter (LFWM) (P=0.043), right parietal white matter (RPWM) (P=0.038), left parietal white matter (LPWM) (P=0.043), right occipital white matter (ROWM) (P=0.016), right caudate nuclei (P<0.001), left caudate nuclei (P=0.003), right putamen (RPUT) (P<0.001), left putamen (P<0.001), right globus pallidus (RGP) (P=0.007), right thalamus (RTHA) (P=0.044), right substantia nigra (RSN) (P=0.019), right dentate nuclei (P=0.033), and left dentate nuclei (P=0.016). Additionally, these patients had significantly lower T2 values in the RPUT (P=0.026), left putamen (P=0.043), RTHA (P=0.026), and left thalamus (LTHA) (P=0.016), along with significantly lower PD values in the RPWM (P=0.045), right caudate nuclei (P<0.001), left caudate nuclei (P<0.001), RPUT (P<0.001), left putamen (P<0.001), RTHA (P=0.016), right red nucleus (RRN) (P=0.016), and left red nucleus (LRN) (P=0.016). Moreover, the platelet count of patients was positively correlated with the T1 and PD values in the caudate nuclei (T1 right: r=0.451, P=0.030; T1 left: r=0.397, P=0.042; PD right: r=0.443, P=0.030; PD left: r=0.476 P=0.030) and putamen (T1 right: r=0.453, P=0.030; T1 left: r=0.400, P=0.042; PD right: r=0.463, P=0.030; PD left: r=0.510, P=0.026). In the QSM study, patients tended to exhibit an increase in magnetic susceptibility value in the ROWM and LTHA.
Conclusions: The measurement of T1 values, T2 values, PD values, and magnetic susceptibility values in deep gray-matter nuclei and white matter could contribute to the early warning of neurological symptoms and monitoring of disease progression in patients with HBV-related cirrhosis. Among these parameters, T1 and PD values may exhibit higher sensitivity as compared to magnetic susceptibility values.
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http://dx.doi.org/10.21037/qims-2024-2969 | DOI Listing |
Trop Doct
September 2025
Additional Professor, Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Chikungunya virus (CHIKV) typically causes febrile illness and arthralgia. However, severe complications such as encephalitis, rhabdomyolysis, and multiorgan dysfunction are increasingly recognised, particularly during epidemics in endemic regions. We report a case of a 61-year old male presenting with progressive flaccid paraparesis and respiratory failure following febrile illness.
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International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
The concept of the central nervous system (CNS) reserve emerged from the mismatch often observed between the extent of brain pathology and its clinical manifestations. The cognitive reserve reflects an "active" capacity, driven by the plasticity of CNS cellular components and shaped by experience, learning, and memory processes that increase resilience. We propose that neuroglial cells are central to defining this resilience and cognitive reserve.
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iInstitut de Mécanique des Fluides de Toulouse (IMFT), Université de Toulouse, CNRS, INPT, Université Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Cerebral Amyloid Angiopathy, a common age-related small vessel disease leading to hemorrhagic stroke, shares many characteristics with Alzheimer's disease: toxic amyloid deposits, microvascular alterations and enlarged perivascular spaces (EPVS). Together, PVS enlargement, reduced amyloid-β clearance and further accumulation form a vicious cycle underlying disease progression. Yet, the neuropathological correlates of EPVS, including the associated angioarchitecture, are poorly understood.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Key Laboratory of Modern Toxicology of Ministry of Education; School of Basic Medical Sciences, Nanjing Medical University, 211166 Nanjing, Jiangsu, China.
Cognitive impairment represents a progressive neurodegenerative condition with severity ranging from mild cognitive impairment (MCI) to dementia and exerts significant burdens on both individuals and healthcare systems. Vascular cognitive impairment (VCI) represents a heterogeneous clinical continuum, spanning a spectrum from subcortical ischemic VCI (featuring small vessel disease, white matter lesions, and lacunar infarcts) to mixed dementia, where vascular and Alzheimer's-type pathologies coexist. While traditionally linked to macro- and microvascular dysfunction, the mechanisms underlying VCI remain complex.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Institute of Neuroscience and Third Affiliated Hospital, Zhengzhou University, 450052 Zhengzhou, Henan, China.
Background: Germinal matrix hemorrhage (GMH) is a common complication of premature infants with lifelong neurological consequences. Inflammation-mediated blood-brain barrier (BBB) disruption has been implicated as a main mechanism of secondary brain injury after GMH. The cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a crucial role in inflammation, yet its involvement in GMH pathophysiology remains unclear.
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