Purpose: To assess whether hippocampal atrophy develops in conjunction with clinical or subclinical epileptiform or encephalopathic activity in subjects with neurocysticercosis (NCC).
Methods: Using a population-based and nested case-control study design, scalp EEGs and brain MRIs were performed in Atahualpa residents aged ≥40 years, who have imaging-confirmed NCC (case patients), as well as in age- and sex-matched NCC-free control subjects.
Results: Sixty-two case patients and 62 control subjects were included. Encephalopathic EEG patterns were more common in five NCC subjects with epilepsy than in those without a history of seizures. Epileptiform EEG activity was noted in one patient with NCC but in none of the control subjects. This subject's focal epileptiform discharges correlated with the location of calcified cysticerci in the brain parenchyma, and the hippocampus ipsilateral to the epileptiform discharges was more atrophic than the contralateral hippocampus. The degree of hippocampal atrophy in patients with NCC without a history of seizures was significantly greater than in control subjects (P < 0.01) and tended to be even greater in patients with NCC with a history of seizures.
Conclusions: Hippocampal atrophy may not be exclusively related to seizure activity in patients with NCC. Other mechanisms, such as recurrent bouts of inflammation around calcified cysticerci, might explain the association between NCC and hippocampal atrophy.
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http://dx.doi.org/10.1097/WNP.0000000000000471 | DOI Listing |
Brain
January 2025
Comprehensive Epilepsy Program, Department of Neurology, University of Virginia, Charlottesville, Virginia 22908, USA.
Seizures in people with dementia (PWD) are associated with faster cognitive decline and worse clinical outcomes. However, the relationship between ongoing seizure activity and postmortem neuropathology in PWD remains unexplored. We compared post-mortem findings in PWD with active, remote, and no seizures using multicentre data from 39 Alzheimer's Disease Centres from 2005 to 2021.
View Article and Find Full Text PDFBrain
January 2025
U1237, Physiopathology and Imaging of Neurological Disorders (PhIND), Neuropresage Team; INSERM, University of Caen Normandy; GIP Cyceron, 14000 Caen, France.
Curing Alzheimer's disease remains hampered by an incomplete understanding of its pathophysiology and progression. Exploring dysfunction in medial temporal lobe networks, particularly the anterior-temporal (AT) and posterior-medial (PM) systems, may provide key insights, as these networks exhibit functional connectivity alterations along the entire Alzheimer's continuum, potentially influencing disease propagation. However, the specific changes in each network and their clinical relevance across stages are not yet fully understood.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Rush University Medical Center, Chicago, Illinois, USA.
Limbic predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is highly prevalent in late life and a common co-pathology with Alzheimer's disease neuropathologic change (ADNC). LATE-NC is a slowly progressive, amnestic clinical syndrome. Alternatively, when present with ADNC, LATE-NC is associated with a more rapid course.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Neuroscience, University of California, Berkeley, California, USA.
Introduction: Successful cognitive aging is related to both maintaining brain structure and avoiding Alzheimer's disease (AD) pathology, but how these factors interplay is unclear.
Methods: A total of 109 cognitively normal older adults (70+ years old) underwent amyloid beta (Aβ) and tau positron emission tomography (PET) imaging, structural magnetic resonance imaging (MRI), and cognitive testing. Cognitive aging was quantified using the cognitive age gap (CAG), subtracting chronological age from predicted cognitive age.
Eur J Neurol
January 2025
Department of Neurosurgery, Medical University of Vienna, Vienna, Austria.
Background: Temporal lobe epilepsy (TLE) can lead to structural brain abnormalities, with thalamus atrophy being the most common extratemporal alteration. This study used probabilistic tractography to investigate the structural connectivity between individual thalamic nuclei and the hippocampus in TLE.
Methods: Thirty-six TLE patients who underwent pre-surgical 3 Tesla magnetic resonance imaging (MRI) and 18 healthy controls were enrolled in this study.
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