Publications by authors named "J Kobal"

Article Synopsis
  • Huntington's disease is a neurodegenerative disorder caused by a mutation in the huntingtin protein, leading to symptoms like chorea and cognitive decline due to neuronal death.
  • Recent research highlights the importance of the neurovascular unit in understanding the disease, particularly the effects of the mutant huntingtin protein on brain function.
  • A study compared presymptomatic and symptomatic Huntington's disease patients to healthy controls, revealing reduced neurovascular phase coherence and lower efficiency of oxygen transport to the brain, indicating impaired neurovascular function in both patient groups.
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The risk of neurodegenerative disorders increases with age, due to reduced vascular nutrition and impaired neural function. However, the interactions between cardiovascular dynamics and neural activity, and how these interactions evolve in healthy aging, are not well understood. Here, the interactions are studied by assessment of the phase coherence between spontaneous oscillations in cerebral oxygenation measured by fNIRS, the electrical activity of the brain measured by EEG, and cardiovascular functions extracted from ECG and respiration effort, all simultaneously recorded.

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Background: Cerebral venous thrombosis (CVT) is a rare cerebral vascular disease, the presentation of which is highly variable clinically and radiologically. A recent study demonstrated that isolated subarachnoid hemorrhage (iSAH) in CVT is not as rare as thought previously and may have a good prognostic significance. Hemorrhagic venous infarction, however, is an indicator of an unfavorable outcome.

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Introduction: The aim of the study was to follow tonic and phasic autonomic nervous activity in Huntington disease (HD) mutation carriers and patients.

Methods: Evaluation of motor functions and total functional capacity was performed in 30 HD mutation carriers or patients at the beginning and in 22 subjects after 8-10 years. Continuous arterial blood pressure, heart rate (HR), and ECG at rest were measured, and HR variability analysis was performed in four different ways.

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Testing for antiphospholipid antibodies could be an important part in determining the cause of a cerebrovascular event (CVE). Currently, it is also unknown whether antiphospholipid antibodies represent a risk factor for the development of a CVE and whether the selected therapy options are efficacious. So, this study aimed at (1) determining the frequency of patients experiencing a CVE and fulfilling the laboratory criterion for an antiphospholipid syndrome (APS), (2) investigating whether the persistent presence of antiphospholipid antibodies represented a risk factor for a CVE, and (3) focusing on the efficacy of the selected treatment strategy in the first year after the CVE.

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